The Center for Immortality Strategies and News

Can we live forever? Kaku, Fahey, de Grey, Tipler on Science Channel

2011-07-27T14:30:00.000-04:00

“Can We Live Forever?” — Through the Worm Hole Season 2, narrated by Morgan Freeman — will air on Science Channel starting Wednesday, July 27, 10 p.m.

Michio Kaku, Thermodynamics; Greg Fahey, Cryogenic Preservation;Aubrey de Grey, Forever Young; Frank Tipler, The Omega Point.
“This popularization is an excellent contribution to convincing the newly arrived cognoscenti that our agenda is not pure fantasy,” said L. Stephen Coles, M.D., Ph.D., Co-Founder, Los Angeles Gerontology Research Group. “Let’s get to Ray’s ‘The Singularity’ ASAP, so we can ‘make it so!’”
Teasers

Originally posted by the editors of Kurzweil news

The Immortality Virus by Christine Amsden book review

2011-06-02T16:41:00.002-04:00

Christine Amsden’s second novel, The Immortality Virus, raises an intriguing question: Is it really all that wonderful to find the secret of immortality and live forever?

It’s the 21st century and the world is being ruled by The Establishment, a totalitarian government made of an elite few. People don’t age any more. As a result, overpopulation has created poverty, hunger, violence, and chaos. People don’t even have empathy for their fellow human beings and cruelty and murder abound. Only the elite few can afford to eat normal food; the rest feed on suspicious, high-protein nutri-bars believed to be made up of human flesh.

At the beginning of the story, our feisty 130-year old PI protagonist, Grace Harper, is hired to complete a mission: she must discover the whereabouts of Jordan Lacklin, the scientist responsible for the ‘virus’ that started The Change about 400 years ago while working on the cure for Alzheimer’s. The secret mission puts Grace’s life in danger. On one side, there are those who want to undo The Change to improve the quality of life and the world; on the other side, there are those who want to keep living forever because they have the means to live in luxury… and they’ll go to extremes to make sure Grace doesn’t complete her mission.

is an entertaining, dystopian/science fiction novel with an interesting premise. Grace Harper is a sympathetic, kick-ass heroine: strong, spirited and opinionated. She also has a kind heart that stands out in the cruel society she inhabits. I personally loved her witty comebacks and quirky sense of humor.

Although the story gets a bit slow somewhere around the middle, Amsden offers enough action, twists and turns to keep most readers turning the pages. The dialogue is crisp and natural and helps to keep the pace moving. Amsden uses a lot of dialogue and action scenes, and keeps description and narration at a minimum. If you love dystopian novels with strong heroines and you’re attracted to the subject of immortality, I recommend you give this one a try.

You can get a copy of it on sale here at amazon The Immortality Virus for only 3.25$!

Original article written by blogcritics.org

Genetics: The Key to Immortality?

2011-06-01T16:36:00.000-04:00

I just found this video on YouTube by Michio Kaku a theoretical physicist that believes within 10 years, everyone will have a digital copy of their genome for just $1000, and by comparing millions of these codes, we may find the cure for aging and many other diseases.

Check out the video here

A Blood Test Offers Clues to Longevity

2011-05-22T05:03:00.000-04:00

Want to know how long you will live?

University of Texas

Telomeres are structures on the tips of chromosomes that shorten as people age.

Blood tests that seek to tell people their biological age — possibly offering a clue to their longevity or how healthy they will remain — are now going on sale.

But contrary to various recent media reports, the tests cannot specify how many months or years someone can expect to live. Some experts say the tests will not provide any useful information.

The tests measure telomeres, which are structures on the tips of chromosomes that shorten as people age. Various studies have shown that people with shorter telomeres in their white blood cells are more likely to develop illnesses like cancer, heart disease and Alzheimer’s disease, or even to die earlier. Studies in mice have suggested that extending telomeres lengthens lives.

Seizing on that, laboratories are beginning to offer tests of telomere length, setting off a new debate over what genetic tests should be offered to the public and what would be the ethical implications if the results were used by employers or others.

Some of the laboratories offering the tests emphasize that the results are merely intended to raise a warning flag.
“We see it as a kind of wake-up call for the patient and the clinician to say, ‘You know, you’re on a rapidly aging path,’ ” said Otto Schaefer, vice president for sales and marketing at SpectraCell Laboratories in Houston, which offers a test for $290.

A company in Spain, provocatively named Life Length, has begun selling a test for 500 euros ($712), that says that it can tell people their biological age, which may not correspond to their chronologic age.

Another company, Telome Health of Menlo Park, Calif., plans to begin offering a test later this year for about $200. It was co-founded by Elizabeth H. Blackburn of the University of California, San Francisco, who shared a Nobel Prize in 2009 for discoveries related to telomeres.

Calvin B. Harley, the chief scientific officer at Telome Health, said the test would be akin to a car’s dashboard signal, a “check engine light.” He compared it with a cholesterol test, but more versatile since it can predict a risk of various illnesses, not just heart attacks.

But among the critics of such tests is Carol Greider, a molecular biologist at Johns Hopkins University, who was a co-winner of the Nobel Prize with Dr. Blackburn.

Dr. Greider acknowledged that solid evidence showed that the 1 percent of people with the shortest telomeres were at an increased risk of certain diseases, particularly bone marrow failure and pulmonary fibrosis, a fatal scarring of the lungs. But outside of that 1 percent, she said, “The science really isn’t there to tell us what the consequences are of your telomere length.”

Dr. Greider said that there was great variability in telomere length. “A given telomere length can be from a 20-year-old or a 70-year-old,” she said. “You could send me a DNA sample and I couldn’t tell you how old that person is.”

Dr. Peter Lansdorp, a telomere expert at the British Columbia Cancer Agency, also had doubts. “If telomeres are short for you or me, what does it mean?” he said. Dr. Lansdorp started a company, Repeat Diagnostics, which conducts telomere testing for medical researchers only.

Recent media reports speculated on the tests and their possible implications, including ethical problems.
“You could imagine insurance companies wanting this knowledge to set rates or deny coverage,” said Jerry W. Shay, a professor of cell biology at the University of Texas Southwestern Medical Center in Dallas, who is an adviser to Life Length.

Test vendors say the speculation is running wild.
“It doesn’t mean we will tell anyone how long they will live,” said María Blasco, a co-founder of Life Length and a molecular biologist at the Spanish National Cancer Research Center in Madrid. Even if a 50-year-old has the telomere length more typical of a 70-year-old, she said, “This doesn’t mean your whole body is like a 70-year-old person’s body.”

Still, she said, “We think it can be helpful to people who are especially keen on knowing how healthy they are.”

Generally tests offered by a single laboratory do not have to be approved by the Food and Drug
Administration. But the F.D.A. has been cracking down recently on some tests offered to the public, saying they may need approval. The FDA said in a statement Wednesday that it was aware of the tests, and had not come to any conclusions.

Executives at both Telome Health and Life Length say they will require a doctor to be involved in ordering the test, though SpectraCell said it allowed individuals to order the test.

To read the rest of the article here at New York Times

PBS documentary"Can We Live Forever"

2011-05-19T17:38:00.000-04:00

I just watched this documentary by PBS called "Can We Live Forever" in which they discuss different ways people are trying to become immortal biologically or non-biologically via artificial organs, suspended animation, gene therapy and avatar replicas of ourselves.

You can watch it for free on the PBS website here http://video.pbs.org/video/1754457671/

Engineering human tissue regeneration

2011-05-14T20:18:00.000-04:00

Engineered tissue constructs can actually induce or augment the body’s own reparative mechanisms, including complex tissue regeneration, researchers at Yale University have found.

The researchers tested whether cells produced in a mouse host’s bone marrow might be a source for new cells. They replaced the bone marrow cells of a female mouse with those of a male mouse and added them to previously designed scaffolds before implanting the graft into female mice.
The researchers found that the cells forming the new vessel were female, meaning they did not come from the male bone marrow cells.

They also implanted a segment of male vessel attached to the scaffold into a female host. After analysis, the researchers found that the side of the graft next to the male segment developed with male vessel wall cells while the side of the graft attached to the female host’s vessel formed from female cells, proving that the cells in the new vessel must have migrated from the adjacent normal vessel.

Ref: Narutoshi Hibino, Gustavo Villalona, Nicholas Pietris, Daniel R. Duncan, Adam Schoffner, Jason D. Roh, Tai Yi, Lawrence W. Dobrucki, Dane Mejias, Rajendra Sawh-Martinez, Jamie K. Harrington, Albert Sinusas, Diane S. Krause, Themis Kyriakides, W. Mark Saltzman, Jordan S. Pober, Toshiharu Shin’oka, Christopher K. Breuer, Tissue-engineered vascular grafts form neovessels that arise from regeneration of the adjacent blood vessel, FASEB Journal, 2011; DOI: 10.1096/fj.11-182246

Richard walker

2011-05-10T22:01:00.000-04:00

I found this video on youtube the other day with Richard Walker from an A4M conference talking about hormone therapy as a cornerstone for antiaging treatments.There are a few other videos by him on youtube also to check out if you are interested after this one if you are so inclined.

http://youtu.be/qM8_zTKJ86c

Tv show Torchwood explores the reality of Immortality

2011-04-11T01:53:00.000-04:00

Torchwood is a British tv show thats a spin off from the Dr. Who. The show's main theme is about a group of alien-hunters from thr future that protect the earth from evil ET's.

Captain Jack Harkness(their leader) is immortal and from the 51st century. Some of the episodes explore the pros and cons of being immortal and a recent episode from season 4 which airs July 8 on Starz addresses what happens when people stop dying on Earth. That's right—what if everyone suddenly became immortal?

check out the teaser here

How Far to Immortality? : Ray Kurzweil

2011-03-28T01:56:00.000-04:00

I just found this video today by Ray Kurzweil discussing how he thinks we will eventually achieve immortality

2045: The Year Man Becomes Immortal

2011-02-13T11:00:00.000-05:00

On Feb. 15, 1965, a diffident but self-possessed high school student named Raymond Kurzweil appeared as a guest on a game show called I've Got a Secret. He was introduced by the host, Steve Allen, then he played a short musical composition on a piano. The idea was that Kurzweil was hiding an unusual fact and the panelists — they included a comedian and a former Miss America — had to guess what it was.

On the show (see the clip on YouTube), the beauty queen did a good job of grilling Kurzweil, but the comedian got the win: the music was composed by a computer. Kurzweil got $200.
(See TIME's photo-essay "Cyberdyne's Real Robot.")

Kurzweil then demonstrated the computer, which he built himself — a desk-size affair with loudly clacking relays, hooked up to a typewriter. The panelists were pretty blasé about it; they were more impressed by Kurzweil's age than by anything he'd actually done. They were ready to move on to Mrs. Chester Loney of Rough and Ready, Calif., whose secret was that she'd been President Lyndon Johnson's first-grade teacher.
But Kurzweil would spend much of the rest of his career working out what his demonstration meant. Creating a work of art is one of those activities we reserve for humans and humans only. It's an act of self-expression; you're not supposed to be able to do it if you don't have a self. To see creativity, the exclusive domain of humans, usurped by a computer built by a 17-year-old is to watch a line blur that cannot be unblurred, the line between organic intelligence and artificial intelligence.

That was Kurzweil's real secret, and back in 1965 nobody guessed it. Maybe not even him, not yet. But now, 46 years later, Kurzweil believes that we're approaching a moment when computers will become intelligent, and not just intelligent but more intelligent than humans. When that happens, humanity — our bodies, our minds, our civilization — will be completely and irreversibly transformed. He believes that this moment is not only inevitable but imminent. According to his calculations, the end of human civilization as we know it is about 35 years away. (See the best inventions of 2010.)

Computers are getting faster. Everybody knows that. Also, computers are getting faster faster — that is, the rate at which they're getting faster is increasing.

True? True.

So if computers are getting so much faster, so incredibly fast, there might conceivably come a moment when they are capable of something comparable to human intelligence. Artificial intelligence. All that horsepower could be put in the service of emulating whatever it is our brains are doing when they create consciousness — not just doing arithmetic very quickly or composing piano music but also driving cars, writing books, making ethical decisions, appreciating fancy paintings, making witty observations at cocktail parties.

If you can swallow that idea, and Kurzweil and a lot of other very smart people can, then all bets are off. From that point on, there's no reason to think computers would stop getting more powerful. They would keep on developing until they were far more intelligent than we are. Their rate of development would also continue to increase, because they would take over their own development from their slower-thinking human creators. Imagine a computer scientist that was itself a super-intelligent computer. It would work incredibly quickly. It could draw on huge amounts of data effortlessly. It wouldn't even take breaks to play Farmville.

Probably. It's impossible to predict the behavior of these smarter-than-human intelligences with which (with whom?) we might one day share the planet, because if you could, you'd be as smart as they would be. But there are a lot of theories about it. Maybe we'll merge with them to become super-intelligent cyborgs, using computers to extend our intellectual abilities the same way that cars and planes extend our physical abilities. Maybe the artificial intelligences will help us treat the effects of old age and prolong our life spans indefinitely. Maybe we'll scan our consciousnesses into computers and live inside them as software, forever, virtually. Maybe the computers will turn on humanity and annihilate us. The one thing all these theories have in common is the transformation of our species into something that is no longer recognizable as such to humanity circa 2011. This transformation has a name: the Singularity.

The difficult thing to keep sight of when you're talking about the Singularity is that even though it sounds like science fiction, it isn't, no more than a weather forecast is science fiction. It's not a fringe idea; it's a serious hypothesis about the future of life on Earth. There's an intellectual gag reflex that kicks in anytime you try to swallow an idea that involves super-intelligent immortal cyborgs, but suppress it if you can, because while the Singularity appears to be, on the face of it, preposterous, it's an idea that rewards sober, careful evaluation.
To read the last 5 pages of Times article

See pictures of cinema's most memorable robots.
From TIME's archives: "Can Machines Think?"
See TIME's special report on gadgets, then and now.

Human Biological Immortality in 50 years

2011-02-01T19:54:00.000-05:00

Posted by Marios Kyriazis in categories: biological, complex systems, futurism

I believe that death due to ageing is not an absolute necessity of human nature. From the evolutionary point of view, we age because nature withholds energy for somatic (bodily) repairs and diverts it to the germ-cells (in order to assure the survival and evolution of the DNA). This is necessary so that the DNA is able to develop and achieve higher complexity.

Although this was a valid scenario until recently, we have now evolved to such a degree that we can use our intellect to achieve further cognitive complexity by manipulating our environment. This makes it unnecessary for the DNA to evolve along the path of natural selection (which is a slow and cumbersome, ‘hit-and-miss’ process), and allows us to develop quickly and more efficiently by using our brain as a means for achieving higher complexity. As a consequence, death through ageing becomes an illogical and unnecessary process. Humans must live much longer than the current lifespan of 80-120 years, in order for a more efficient global evolutionary development to take place.

It is possible to estimate how long the above process will take to mature (see figure below). Consider that the creation of the DNA was approximately 2 billion years ago, the formation of a neuron (cell) several million years ago, that of an effective brain (Homo sapiens sapiens) 200 000 years ago, and the establishment of complex societies (Ancient Greece, Rome, China etc.) thousands of years ago. There is a logarithmic reduction of the time necessary to proceed to the next more complex step (a reduction by a factor of 100).

This means that global integration (and thus indefinite lifespans) will be achieved in a matter of decades (and certainly less than a century), starting from the 1960s-1970s (when globalisation in communications, travel and science/technology started to became established). This leaves another maximum of 50 years before the full global integration becomes established.

Each step is associated with a higher level of complexity, and takes a fraction of the timein order to mature, compared to the previous one.

1. DNA   (organic life – molecules: billions of years)
2. Neuron   (effective cells: millions of years)
3. Brain   (complex organisms – Homo sapiens: thousands of years)
4. Society (formation of effective societies: several centuries)
5. Global Integration (formation of a ‘super-thinking entity’: several decades)

Step number 5 implies that humans who have already developed an advance state of cognitive complexity and sophistication will transcend the limits of evolution by natural selection, and therefore, by default, must not die through ageing. Their continual life is a necessary requirement of this new type of evolution.

For full details see:
https://acrobat.com/#d=MAgyT1rkdwono-lQL6thBQ

'Un-growth hormone' increases longevity

2011-01-26T14:50:00.000-05:00

A compound which acts in the opposite way as growth hormone can reverse some of the signs of aging, a research team that includes a Saint Louis University physician has shown. The finding may be counter-intuitive to some older adults who take growth hormone, thinking it will help revitalize them.

Their research was published in the Dec. 6 online edition of the Proceedings of the National Academy of Sciences.

The findings are significant, says John E. Morley, M.D., study co-investigator and director of the divisions of geriatric medicine and endocrinology at Saint Louis University School of Medicine, because people sometimes take growth hormone, believing it will be the fountain of youth.

"Many older people have been taking growth hormone to rejuvenate themselves," Morley said. "These results strongly suggest that growth hormone, when given to middle aged and older people, may be hazardous."
The scientists studied the compound MZ-5-156, a "growth hormone-releasing hormone (GHRH) antagonist." They conducted their research in the SAMP8 mouse model, a strain engineered for studies of the aging process. Overall, the researchers found that MZ-5-156 had positive effects on oxidative stress in the brain, improving cognition, telomerase activity (the actions of an enzyme which protects DNA material) and life span, while decreasing tumor activity.

MZ-5-156, like many GHRH antagonists, inhibited several human cancers, including prostate, breast, brain and lung cancers. It also had positive effects on learning, and is linked to improvements in short-term memory. The antioxidant actions led to less oxidative stress, reversing cognitive impairment in the aging mouse.

William A. Banks, M.D., lead study author and professor of internal medicine and geriatrics at the University of Washington School of Medicine in Seattle, said the results lead the team "to determine that antagonists of growth hormone-releasing hormone have beneficial effects on aging."

Provided by Saint Louis University

Advances in 3DvBrain Scanning for Mind Uploading

2011-01-16T17:45:00.000-05:00

Microscope records firing of thousands of individual neurons in 3-D

UCLA neuroscientists have now collaborated with physicists to develop a non-invasive, ultra–high-speed microscope that can record in real time the firing of thousands of individual neurons in the brain as they communicate, or miscommunicate, with each other.

“In our view, this is the world’s fastest two-photon excitation microscope for three-dimensional imaging in vivo,” said UCLA physics professor Katsushi Arisaka, who designed the new optical imaging system with UCLA assistant professor of neurology and neurobiology Dr. Carlos Portera-Cailliau and colleagues.
Their research appears in the Jan. 9 edition of the journal Nature Methods.

Because neuropsychiatric diseases like autism and mental retardation often display no physical brain damage, it’s thought they are caused by conductivity problems — neurons not firing properly. Normal cells have patterns of electrical activity, said Portera-Cailliau, but abnormal cell activity as a whole doesn’t generate relevant information the brain can use.

“One of the greatest challenges for neuroscience in the 21st century is to understand how the billions of neurons that form the brain communicate with one another to produce complex behaviors,” he said. “The ultimate benefit from this type of research will come from deciphering how dysfunctional patterns of activity among neurons lead to devastating symptoms in a variety of neuropsychiatric disorders.”

For the last few years, Portera-Cailliau has been using calcium imaging, a technique that uses fluorescent dyes that are taken up by neurons. When the cells fire, they “blink like lights in a Christmas tree,” he said. “Our role now is to decipher the code that neurons use, which is buried in those blinking light patterns.”
But that technique had its limitations, according to Portera-Cailliau.

“The signal of the calcium-based fluorescent dye we used faded as we imaged deeper into the cortex. We couldn’t image all the cells,” he said.

Another problem was speed. Portera-Cailliau and his colleagues were concerned they were missing information because they couldn’t image a large enough portion of the brain fast enough to measure the group-firing of individual neurons. That was the driving impulse behind the collaboration with Arisaka and one of his graduate students, Adrian Cheng, to find a better way to record neuronal activity faster.

The imaging technology they developed is called multifocal two-photon microscopy with spatio-temporal excitation-emission multiplexing — STEM for short. The researchers modified two-photon laser-scanning microscopes to image fluorescent calcium dyes inside the neurons, and came up with a way to split the main laser beam into four smaller beamlets. This allowed them to record four times as many brain cells as the earlier version, or four times faster. In addition, they used a different beam to record neurons at different depths inside the brain, giving a 3-D effect, which had never been done previously.

“Most video cameras are designed to capture an image at 30 pictures per second. What we did was speed that up by 10 times to roughly 250 pictures per second,” Arisaka said. “And we are working on making it even faster.”

The result, he said, “is a high-resolution three-dimensional video of neuronal circuit activity in a living animal.”
The use of calcium imaging in research is already providing dividends. Portera-Cailliau studies Fragile X syndrome, a form of autism. By comparing the cortex of a normal mouse with a Fragile X mutant mouse, his group has discerned the misfiring that occurs in the Fragile X brain.

Adapted from materials provided by UCLA

A Test for 400 Inherited Diseases

2011-01-15T19:36:00.000-05:00

Spotting disease: The white column in the middle of this DNA sequence chart highlights a four-letter deletion in the genome that is linked to a disorder called Lesch-Nyan syndrome. The disorder, which strikes in infancy, causes severe mental and physical problems.

New technology will allow broad screening for prospective parents.

Researchers have developed a new test designed to simultaneously detect genetic mutations involved in more than 400 severe diseases. The test, which was shown to be highly accurate, is initially aimed at screening prospective parents for mutations linked to rare inherited disorders.

Thanks to inexpensive sequencing technology, scientists aim to offer the test for just a few hundred dollars, similar to the cost of tests currently available for detecting individual diseases or a handful of disorders.

"We want this test to become available in the same way Tay-Sachs and cystic-fibrosis testing has," says Stephen Kingsmore, chief scientific officer of the National Center for Genome Resources and senior author on the study. Tay-Sachs, a rare inherited disorder, strikes in infancy and is typically fatal within the first few years of life. "Forty years of experience with Tay-Sachs resulted in that awful disorder becoming pretty much eradicated in North America," he says. "This is just on a grander scale."

The new test, which reads the sequence of about 2 million letters of DNA spread out over 7,000 different chunks, is designed to detect mutations in genes that have been linked to so-called recessive Mendelian disorders, including cystic fibrosis and Tay-Sachs. People who inherit two mutant copies of the relevant gene are guaranteed to develop the disease, while people with only one copy will not. These diseases often strike early in life with severe consequences, including severe disability and death. And while they are individually rare, together they account for about 20 percent of infant mortality.

Testing prospective parents for these mutations can help them prevent or plan for the diseases. Couples who are both carriers of mutations in a particular disease-linked gene could choose to adopt, to conduct genetic tests on in-vitro-fertilized embryos, or to do prenatal testing and terminate affected pregnancies.
While more than 1,000 genes have been linked to recessive Mendelian disorders, the tests now available to prospective parents screen for only the most common, such as cystic fibrosis, and are mainly offered to parents in high-risk groups. Ashkenazi Jews are at particular risk of carrying Tay-Sachs mutations, for example.

"To be able to screen for more than 400 rare conditions is really an important advance," says Eric Topol, director of the Scripps Translational Science Institute, who was not involved in the study. "We don't have anything near that today."

The major impediment to broad genetic screening has been cost, for the kind of DNA sequencing used in most clinical diagnostic tests is very expensive. Kingsmore and collaborators took advantage of the latest sequencing technology, which can sequence much greater volumes of DNA more quickly and cheaply. This technology has already transformed genetic research, but it has been slow to make its way into medical use.
"A huge question is whether it is robust enough to be used in clinical testing in humans," says Kingsmore.

According to his findings, published Wednesday in Science Translational Medicine, the answer is yes. When compared with another technology—microarrays designed to detect specific genetic mutations—the sequencing-based approach was 99.98 percent accurate. And follow-up testing of DNA from 100 people with a known mutation was 100 percent accurate. (Kingsmore's team actually found that a number of the original samples had been misclassified.)

The advantage of a sequencing-based test over one that uses microarrays is that the latter can detect only known mutations. Sequencing, on the other hand, can spot any variation in disease-linked genes, even if it has never been seen before. (For some diseases, a few common mutations account for most cases of the disease, but for others, many different types of mutations can disrupt the relevant gene.) A comprehensive screening test launched last year by a startup called Counsyl tests only for known mutations. That's a problem, says Kingsmore, because "we don't have a good catalogue of mutations for most diseases."

To develop the new test, the team modified existing technology to select relevant portions of the genome by binding stretches of complementary DNA to the regions of interest, drawing them out of a soup of DNA. Next they used sequencing technology from Illumina to analyze the extracted DNA. Since submitting their paper, the researchers have expanded the test to scan for mutations linked to more than 600 different conditions.

Kingsmore says the test currently costs $618 to run, not including any costs associated with commercialization. He predicts the cost will drop in next the next two years. His institute, a nonprofit that developed the technology with funding from a patient-advocacy group, aims to offer it for $500, on par with current carrier screens.

"Rapid progress in sequencing makes it possible to gather the enormous amount of sequencing information at a manageable cost," says Arthur Beaudet, chair of the department of Molecular and Human Genetics at Baylor College of Medicine, who was not involved in the study. "And it will quite likely get cheaper over time."

The test isn't yet available to prospective parents. Researchers are now beginning to test the technology in clinical labs, a necessary step toward getting it approved by the Food and Drug Administration. "We believe we will be able to offer it on a research basis in the summer of 2011," says Kingsmore.

original article by emily singer in technology review

Aging Ills Reversed in Mice

2011-01-14T14:40:00.000-05:00

Scientists Tweak a Gene and Rejuvenate Cells, Raising Hopes for Uses in Humans

By GAUTAM NAIK

Scientists have partially reversed age-related degeneration in mice, an achievement that suggests a new approach for tackling similar disorders in people.
By tweaking a gene, the researchers reversed brain disease and restored the sense of smell and fertility in prematurely aged mice. Previous experiments with calorie restriction and other methods have shown that aspects of aging can be slowed. This appears to be the first time that some age-related problems in animals have actually been reversed.

View Full Image

Dana-Farber Cancer Institute

Two mice involved in an experiment on age-related degeneration. Mice whose telomerase gene was activated showed notable improvements.

"These mice were equivalent to 80-year-old humans and were about to pass away," says Ronald DePinho, co-author of the paper and a scientist at Dana-Farber Cancer Institute in Boston. After the experiment, "they were the physiological equivalent of young adults."

The institute is a teaching affiliate of Harvard Medical School. The first author of the study is Mariela Jaskelioff at Dr. DePinho's lab.

Although the finding is compelling, it remains to be seen whether the approach can slow the signs and symptoms of aging in people. The latest results were obtained with mice that were specifically altered to age prematurely. And while the animals showed no signs of tumors, there is a risk that the technique could trigger cancer.

The experiment focused on telomerase, an enzyme that makes small units of DNA that seal the tips of chromosomes. These DNA units, known as telomeres, act like the plastic caps at the ends of a shoelace, preventing the chromosomes from fraying and the genes inside them from unraveling. In 2009, three U.S. scientists won the Nobel Prize in medicine for illuminating the mysteries of telomerase.

New Lease on Life

How scientists partly reversed age-related degeneration in mice

Scientists engineered prematurely aged mice that developed age-related problems; testes produced little sperm, brains stopped producing new cells and sense of smell atrophied.
They injected the mice with a drug that switched on a gene, which stimulated telomerase production. That lengthened the telomeres that cap the ends of chromosomes and keep them from fraying.
In the treated mice, their testes produced new, viable sperm cells, their brains began producing new cells and their sense of smell returned.
The treated animals went on to have a typical lifespan, though they didn't live longer than normal mice.

Many different stimuli conspire and contribute to the aging process. The telomere is just one of them and likely not the most dominant. In normal tissue, telomeres get progressively shorter as part of the aging process, causing cells to stop dividing. As a result, stem cells go into a state of quiescence, organs atrophy and brain cells die.

As people age, low levels of telomerase are linked to the erosion of telomeres. Dr. DePinho and his colleagues wanted to see if by reactivating telomerase in mice they could halt—or possibly reverse—the shortening of telomeres, and thus turn back the clock on some aspects of aging.
The team made genetically engineered mice that aged prematurely. The animals had short, dysfunctional telomeres and suffered a range of age-related problems. Their spleens were atrophied, their intestines were damaged, and the sense of smell was impaired.

The brains were also shrunken, and the animals were incapable of growing new brain cells. Male mice had smaller-than-normal testes and produced depleted amounts of sperm.

"We stacked the deck against us and asked: Is there a point of no return?" said Dr. DePinho.
The researchers had devised an estrogen-based drug that would switch on the animals' dormant telomerase gene, known as TERT. The drug, in the form of a time-release pellet, was inserted under the skin of some mice. A similar pellet without the active drug was given to a separate group of control mice.
A month later, the treated mice showed surprising signs of rejuvenation. Overall, their telomeres had lengthened and the levels of telomerase had increased. This woke up the dormant brain stem cells, producing new neurons. The spleen, testes and brain grew in size.

In addition, key organs started to function better. The treated mice regained their sense of smell. The male animals' once-depleted testes produced new sperm cells, and their mates gave birth to larger litters. The treated animals went on to have a typical lifespan, though they didn't live longer than normal mice.
The reversals of age-related decline seen in the animals "justify exploration of telomere rejuvenation strategies for age-associated diseases," the paper concludes.

One worry is cancer. Tumors somehow turn on the telomerase gene, allowing cancer cells to divide continuously. Up to 90% of human cancers require certain levels of telomerase to do so. Indeed, many researchers are trying to deactivate telomerase as a cancer-fighting strategy.
Still, turning on telomerase for controlled periods of time might be useful. The strategy might one day have a role in treating rare genetic disorders that are linked to telomeres and cause premature aging, such as Werner's syndrome, according to Dr. DePinho.

The telomerase technique may also be relevant for people who age normally—provided it is clear that prolonged telomerase reactivation doesn't trigger tumors in later life.

Statistically, people with longer telomeres in their blood cells have an increased number of healthy years beyond the age of 60, Dr. DePinho said. And those over 60 with the shortest telomeres have higher rates of diabetes, cardiovascular disease and Alzheimer's.

Dr. DePinho said the next step was to try the technique on normally aged mice to see whether it can slow, halt or reverse signs of aging in them.

Write to Gautam Naik at gautam.naik@wsj.com

The secrets of long life

2011-01-13T16:18:00.000-05:00

The quest may no longer be for the elixir of immortality but with an ageing population there is increased awareness of what it takes to live long and well, writes Dionne Christian.

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Betty McPherson says trying new activities keeps her young. Photo / Richard Robinson

So you've just returned home from a brisk early morning walk with the family - which followed a breakfast of high-fibre, low-sugar cereal topped with fresh fruit and acidophilus yoghurt.

It is the weekend and you're conscious of the need for work/life balance, so now you'll do some gardening with the kids before the babysitter arrives and you join friends for dinner.

You'll probably order chicken, skin removed, of course, with a brown rice pilaf. You may have a glass of wine. One glass, that's your limit. You rarely drink more than that and as for smoking, you threw away the ciggies a decade ago.

Besides, you don't want to be out too late. The whole early to bed, early to rise makes you healthy, wealthy and wise is an adage you like to live by. Obviously the wealthy part appeals but so does the healthy, especially when it comes to longevity.

You can't imagine a world without you in it so you're planning to live as well and long as possible. The title of Roger Hall's play Who Wants To Be 100? (Anyone Who's 99) resonates strongly because you want a telegram from the Queen. Or King. That's if the monarchy outlasts you.

But will the exercise, the healthy diet, reducing your alcohol intake and quitting smoking really help you achieve wrinkles with twinkles? While the experts strongly believe health measures aid longevity, no one actually knows what it takes to live a long life in New Zealand.

In our youth-obsessed and death-defying society, there has never been a detailed study into how and why some New Zealanders live longer. International research can only tell us so much.

Now researchers from the University of Auckland are recruiting 1000 "golden oldies" to take part in an ambitious and far-reaching study to learn how and why some of us survive to a ripe old age.

The Lilacs NZ (take a breath and say it slowly: Life and Living in Advanced Age: A Cohort Study in New Zealand, Te Puawaitanga o Nga Tapuwae Kia Ora Tonu) longitudinal study aims to interview 600 Maori aged 80-90 and 600 non-Maori aged 85 from the Bay of Plenty - that's the Tauranga, Rotorua, Whakatane and Opotiki areas.

Participants undergo a detailed interview, a free health assessment including a blood pressure check, and give blood to determine biological markers of ageing such as cholesterol and homocysteine levels.

Researchers will then visit participants during the next 10 years to follow changes in their lives and to see if they can discover the "secrets to longevity" by comparing results from those who make it most or all of the way through the study with those less fortunate souls.

The Bay of Plenty was chosen because of its diversity and large Maori population. Rotorua is in a geothermal area, has a stable population and an economy based around tourism and primary production. Opotiki, Te Kaha and Whakatane are by the sea, while inland settlements have a forestry focus and Tauranga is a growth area. Findings will be used to develop local and national policies for older people throughout the entire country.

Older people have been defined as those aged 65 and over but the Lilac team say it is of limited use to homogenise all senior citizens like that. After all, there's likely to be a world of difference between a 65-year-old and someone of 87 years.

According to the 2006 Census, there were 495,600 New Zealanders aged 65 and over - up 45,200 on the 2001 Census - with 75 the median age for women and 73.4 the median age for men.

Of more significance is the growth in the number of those aged 85 and over. The number of New Zealanders in that demographic is expected to more than quadruple from just under 57,000 in 2006 to 322,000 by 2051.
So informed debate needs to happen on issues like employment and retirement, raising the pension age, healthcare, ageing in place - as opposed to in rest homes or hospitals - living standards, well-being and the quality of life our senior citizens have.

But lead researchers Ngaire Kerse, Lorna Dyall, Mere Kepa and Karen Hayman, don't want the debate limited to cost benefit analysis or dry financial facts and figures.

While there are questions about nutrition, physical fitness and health in the Lilacs questionnaire, researchers also want to know more about the mental, social, spiritual and family aspects of life and the environment around people as they age.

"Society is focused on the young," says Kepa, who looked after her father in his senior years. "It's a liberal society with the emphasis on rights rather than the co-existing responsibilities that come with those rights. After all, we don't live in this world on our own. Now we are an ageing society, it's about time we started thinking more about our obligations in respect of our elders and finding out more about what it means to be elderly."

Kerse firmly believes the study should consider how the elderly can share their wealth of knowledge and experience with younger generations and, in turn, be accorded greater respect.

"I like to put it like this, 'who makes your Christmas cake?' If you've got a grandmother, an elderly aunt or an ageing mother, I bet it's one of them."

Kerse says the contribution elderly people make to the volunteer sector, for example, and to family in general is often overlooked. A professor of General Practice and Primary Health at the University of Auckland's School of Population Health, she works at a GP practice in Herne Bay and has long been interested in maximising health for older people.

Kerse credits her grandmother, Agnes Hodge, with teaching her to value older people. She recalls with great fondness childhood holidays spent driving from her Southland home to Hodge's home in Motueka.
"She had a magnificent vegetable garden and orchard - plums, raspberry vines and wild strawberries. She just knew so much and was so self-sufficient. She was pretty much independent right up until she died, aged 95. It is so important to maximise health for older people so they can enjoy the last years of their lives to the full, because they have a right to it."

Study participant Ina Benbow is a former accounting and economics teacher. Now 86, she retired in 1978 aged 55 but started voluntary and community-based work, particularly for the SPCA and later for the Heart Foundation.

Happily living in her own home, with a dog and cat for company and a good social life, Benbow's garden is immaculate and her cooking divine. She is almost self-sufficient in her garden, saying it provides a chance for physical activity. A couple of days before her Canvas interview, Benbow was collecting for the Cancer Society's Daffodil Day.

She always wanted to contribute to the world. Volunteer work for her favourite charities was a way to do that and to step out of her comfort zone. Trying new activities - the "Just Do It" philosophy - is one of the many things she believes keeps her young.

"People talk about having a 'bucket list' when you get old," Benbow says, in reference to the movie comedy about two elderly men who devise a list of everything they want to do before they "kick the bucket".
"I think everyone, no matter what their age, should have a bucket list of goals and dreams. I had one right from the time I was a teenager. I wanted to leave Temuka [her hometown] and to see the world and growing up during the Depression, I thought there had to be a better way of life."

In 2000, when she was 76, Benbow put her charity work on hold. She sold up, bought a four-berth motorhome and embarked on a four-year journey around New Zealand. She also motorhomed around Australia and took trips to China, Russia and the rest of Europe.

"Forget about your age, I like to say, because it's only a number on a piece of paper. But with a lot of people, well, they almost become obsessive about being old. They might want to do things, to try something different but just will not.

"It isn't that they cannot, it's that they won't and there is a world of difference between can't and won't. I think it's good to step out of your comfort zone, to challenge yourself. The world really is your oyster and it's up to each individual to make the most of what they have and what they can do."

She says from a budget point of view, her excursion around New Zealand made sense. Most nights she stayed at holiday parks for around $10 a night.

"Everyone needs to learn how to budget," she says. "It's especially true when you're elderly but it's not what you earn, it's what you spend that counts."

Ask Retirement Commissioner Diana Crossan how much money you need to enjoy your last few years and she says it's like asking how long is a piece of a string. The answer depends on who you are and what type of lifestyle you have and want. Crossan says a realistic figure is about 70 per cent of what you earned before retiring.

"Some people panic when they see how much they need but it comes down to making choices. You have to ask questions like, 'do I want an overseas trip each year?' and 'what if I have unexpected medical expenses?"'
She says the time to start thinking about saving for retirement is when you first enter the workforce but she acknowledges that's extremely difficult for many of us to even consider.

"You're 18, you've just started work and you've got money for the first time. You simply can't conceive of being 80 and worrying about money."

Crossan recommends checking out the Retirement Commission's website retirement.org.nz and finance site sorted.org for advice on how to get started with retirement savings and other budgeting tips.

It wasn't money worries alone that got Betty McPherson, 75, thinking about how she wanted to spend her senior years. It was a combination of concern about the impact poor health might have on her and her family.
When McPherson was 49, her husband, then St Stephens School principal Frank "Scotty" McPherson, died unexpectedly of an undiagnosed heart condition. He was 50. The couple had been together since they were teenagers in Northland and married when she was just 18.

"When Scotty died, I didn't want to go on living. I kept working, going through the motions, but I didn't really care about myself. Then one day it hit me that I could go on living for years and if I didn't look after myself, I would not have a good end to my life and would be reliant on others to take care of me."

So McPherson started swimming, walking and dieting. She still watches what she eats and exercises daily. Her health issues are limited to rheumatoid arthritis and a heart fibrillation problem, which is controlled by medication.

"I'm always telling people that when they go to the doctor, they have to take the medication they are prescribed and follow the doctor's instructions. I mean, do they want to live or die?"

McPherson works in Pukekohe as a resource teacher for learning and behaviour. She helps schools turn around the lives of kids with behavioural or learning problems and simply cannot imagine retiring. "I like making good friends with the families I work with and making a difference in children's lives."

A mother of eight - nine, if you include the nephew she helped raise - McPherson became involved with Lilacs through the Ropu Kaitiaki o Nga Tikanga Maori (Maori governance). The group is working with the University of Auckland team to ensure appropriate protocols are followed with Maori participants.

"There is still an eight to 10-year disparity in life expectancy between Maori and non-Maori," says Kerse. "We can't deny that disparity and therein lies a whole lot of other questions."

McPherson believes part of the problems lies in the fact Maori have moved from the country into cities and, by doing so, abandoned healthier lifestyles.

"People were on their own lands, growing or gathering their own food and getting a lot more exercise in the process. I remember when I was a child doing all that stuff. My grandmother taught us how to collect karaka berries, boil them in a big pot of water then steep them in running water for two weeks, then dry them. They were like our peanuts."

Dr Carol Wham, Lilacs co-investigator and senior lecturer at Massey University's Institute of Food Nutrition and Human Health, believes it's never too late to improve eating habits and this can help with health and well-being.

She says it is vital to maintain a healthy weight and keep active to prevent age related decline in muscle mass.
"Age has an important impact on body composition. There is an inevitable loss in lean mass - skeletal muscle and bone - with ageing and a relative increase in body fat. However, the requirements for most nutrients are not reduced, which means foods with a higher nutrient density should be preferred."

Wham says age-related decline in muscle mass, known as sarcopenia, results from genetic and environmental factors and speeds up after 80 years of age. The main effect is reduced muscle strength, which can cause general physical decline and mobility and balance issues.

Likewise, gastrointestinal function and absorption functions decline with age, as can taste. Medications taken for other conditions may impair taste and smell and affect food intake.

But the number one reason for age-related weight loss is depression, especially after losing a spouse. Food and eating have social meaning and eating with others helps enhance nutrient intake.

Not surprisingly, McPherson and Benbow cannot stress enough the importance of staying socially engaged.
"It can be very hard to come to terms with getting older, seeing the people around you pass away, but try to keep on making new friends, preferably younger ones, and try to hang on to your sense of humour," says Benbow.

South African-born long-time Otago resident Don Morrison is soon to turn 81. The father of six and grandfather to 12 says we need to see ourselves as having a more symbiotic relationship with the world around us.

"Perhaps it's because I grew up in Africa, I believe the world - the environment and the people in it - is a closed system where everything is related to everything else and dependent on things staying in balance. I think life should be about respecting and trying to maintain balance within those relationships in the community and the wider environment. I'm not a person who believes in an after-life or anything like that but I think your influence lives on, so you should make sure it's positive."

Like many older New Zealanders, Morrison is no longer in paid employment but like nearly one-fifth of those aged 65 and over, he is active in community and voluntary work.

A former physical education teacher, he helps a local primary school with its "Grandparents Programme", acting as a mentor for pupils. He assists with the Police Blue Light youth mentoring scheme and is a trail boss for the annual Otago Goldfields Cavalcade.

Since 1991 the Otago Goldfields Heritage Trust - of which Morrison is a life member - has organised the event for horse riders, wagoners and walkers. They trek across the country and hills of Otago to a host town, re-tracing the steps of gold miners who sought their fortune at the end of the 19th century.

As a Walking Trail Boss, it is Morrison's job to walk the proposed route of his trail, checking everything is in order, gaining permission from landowners to traverse their properties, arranging accommodation and catering and preparing a budget. He then leads the group on the trail.

No surprise then that when Morrison is not taking care of his 4ha garden property he's out walking, either on his own, with the Clyde Off-Road Walking Group or as a leader of the Milton Rotary Tramping Club, which attracts a fair number of its participants from the North Island.

"I live 4km from the nearest town but I seldom use a car. I prefer to go by bicycle or walk. I love walking, it's my hobby. I've always kept myself fit and I've never drank or smoked, mainly because I couldn't afford it."
Grant Schofield, Professor of Public Health at Auckland University of Technology and director of its Centre for Physical Activity and Nutrition Research, describes Morrison's physical activities as excellent.
Schofield believes maintaining social connections and keeping active are the two most important things we can do to live long and healthily.

"The interesting point is that those two things tend to happen in tandem. If you're active in your senior years, it's likely you are doing so with other people."

He can point to numerous studies showing the positive effects of exercise on physical health - the "use it or lose it" philosophy - but extends that to mental health. For example, exercise improves circulation and that's good for your brain which occupies two per cent of the body but uses 25 per cent of its energy.
"A healthy mind depends a lot of keeping yourself in good shape."

He says one of the most convincing studies about the benefits of physical activity was a 21-year investigation in the United States. Beginning in 1984, researchers sent an annual questionnaire to 538 members of a nationwide running club and 423 healthy, but not so active, California residents. All were aged 50.

Each year, they answered questions about running and exercise frequency, body mass index and disabilities. A total of 284 runners and 156 non-runners completed the 21-year follow-up. The runners were younger in terms of biological markers for age, leaner, less likely to smoke and - importantly - more likely to be alive.
The conclusion? Vigorous exercise at middle and older ages is associated with reduced disability in later life and a notable survival advantage. "If there was a drug that made this much difference to the quality of life, it would be the best thing ever invented," says Schofield.

In August, Lilac received a further $1.2 million grant to enable interviews after one and two years and to examine the impact of dementia.

By Dionne Christian
Originally posted in the

Health Tips | Starting the New Year right

2011-01-01T12:39:00.002-05:00

December 30, 2010 by David Despain

Healthy Aging

Exercising regularly and taking vitamin D may be the two most successful ways to prevent falling in old age, because they help keep muscles and bones stronger [Annals of Internal Medicine]. Staying physically active while pregnant can also help you maintain a healthy body weight after pregnancy while helping you keep blood pressure and blood sugar under control [BJOG].
People who are overweight or obese may need to take more vitamin D because excess fat can interfere with its proper absorption, leading to low vitamin D levels and increased risk of chronic diseases such as osteoporosis, cardiovascular disease and cancer [J of Nutr].
Cutting stroke risk involves reducing sodium (heavy in processed foods), refined sugars, and saturated fats, and increasing potassium (in fruits and vegetables) and low-fat dairy products. If you have diabetes or are otherwise at high risk, experts advise asking your doctor for proper treatment for blood pressure, cholesterol, and coagulation [Stroke]. Eating as least three servings of fish per week can reduce risk of stroke significantly [AJCN], but eating red meat and processed meats (both typically high in saturated fat, cholesterol, and sodium) may increase risk of stroke [Stroke].
Smokers who are screened early for lung cancer can cut their risk of dying from the disease significantly [Lung Cancer].

Healing Foods

A Mediterranean-style diet could save your brain because it includes foods (like vegetables, fish, and olive oil) that help slow cognitive decline [AJCN].
During menopause, soy’s natural content of estrogen-like compounds called isoflavones can be helpful for reducing hot flashes with low risk of breast cancer [AJCN]. Soy also naturally lowers total and LDL cholesterol because of sterols that increase excretion of bile acids [J Clin Lipid].
Salmon can be a natural therapy for ulcerative colitis. Its long-chain omega-3 fatty acids have a natural anti-inflammatory effect that soothes symptoms [Scand J Clin Lab Invest].
Dairy products may reduce risk of diabetes because of a natural fatty acid called trans-palmitoleic acid, which is linked to lower insulin resistance [Annals of Internal Medicine].
Eating dark (no milk) chocolate may be good for the gut. It contains compounds called flavanols that act as “prebiotic” food for fueling the growth of probiotic bacteria in the intestine [AJCN (funded by Mars)].

Social networks

Maintaining a vibrant social life leads to fewer problems dealing with emotional challenges [Stanford]. Can’t get out? No problem. Indoor plants can contribute to a sense of wellbeing and personal satisfaction [HortScience].

2010-12-29T15:50:00.000-05:00

Twitter: Jsun07

Many artificial food dyes should be banned because they pose cancer risks http://tiny.cc/suhiy

Alcor Life Extension Foundation Names Max More, PhD, as Chief Executive Officer

2010-12-27T15:21:00.001-05:00

The Board of Directors of Alcor Life Extension Foundation announced on Dec. 24 that Dr. Max More, 46, has been named Chief Executive Officer effective Jan 1, 2011.

An internationally recognized advocate of the effective and ethical use of technology for life extension and cryopreservation, Dr. More brings experience in running non-profit organizations, many years of analyzing and writing about business organizations, and a long commitment to Alcor’s mission.

More joined Alcor in 1986 as its 67th member, founded Alcor-UK (originally Mizar Limited) in the same year, and has participated in several cryopreservations. He has spoken on cryonics and life extension at numerous conferences and in many national and international media, including a CNN Crossfire debate shortly after the cryopreservation of baseball legend Ted Williams.

“Max brings a quarter century of experience in and commitment to cryopreservation, life extension, and improving the future,” said Alcor director Tim Shavers, “and has earned a reputation for both practical and principled leadership and bold thinking. Crucially, he shares our vision of Alcor’s mission and understands the organization’s past and its challenges and opportunities. His extensive knowledge of our operations, goals, and needs makes him the ideal choice to lead Alcor as CEO.”

More built Extropy Institute, an educational non-profit organization that created the modern transhumanist movement, whose goals centrally include extending healthy human life span. More organized and chaired five successful conferences and, along with Ray Kurzweil, was the keynote speaker at an online summit that lead to the development of the “Proactionary Principle,” and was editor-in-chief of the pioneering publication, Extropy: The Journal of Transhumanist Thought. More’s advocacy of cryonics dates to several years before he became an Alcor cryopreservation member in 1986 while a student at England’s Oxford University. His commitment was reflected academically in his doctoral dissertation, a chapter of which argued for a reconceptualization of death according to which cryopreserved patients are neither fully alive nor dead but in a third state.

“I am honored to assume the leadership of Alcor and to continue the legacy of commitment to maintaining Alcor’s patients in cryopreservation while growing the organization and improving our technological capabilities,” said More. “Since I joined, Alcor has grown from 67 members to around 930, and its patients from 6 to 102. I am thrilled to work with Alcor’s Board, with its broad and deep expertise, to continue and accelerate that growth while keeping a primary focus on protecting our existing patients. I am also committed to strengthening the stability of the organization to better endure over the coming decades and to continuing to raise the level of our medical professionalism and business practices.”

Alcor Life Extension Foundation is a not-for-profit research organization founded in 1972. Alcor is the world leader in cryonics, and cryonics technology. Cryonics is the science of using ultra-cold temperatures to cryopreserve humans. The intent is that advanced scientific procedures may one day be able to revive cryopreserved humans and restore them to good health. Alcor performed its first human cryopreservation in 1976, and has engaged in long-term care of cryopreserved members in its state-of-the-art facility since then.
Among the scientific achievements of Alcor is the use of advanced cryoprotectant formulas capable of vitrification. Vitrification enables cryopreservation to take place without the damage that occurs in freezing tissue. Alcor has published papers in scientific journals documenting the quality of tissue preservation possible with its procedures, and the effects of clinical death on the brain. Alcor also sponsors research in the field of nanomedicine, a technology that may someday be used to revive cryopreserved patients.

Alcor is overseen by a Board of Directors consisting of successful and well-regarded scientists, physicians, attorneys, and other professionals. Alcor also has a group of scientific advisors, who are leaders in the fields of medical research, nanotechnology, and computer science.

Adapted from materials provided by Alcor Life Extension Foundation

Download Your Brain... Death Defeated?

2010-12-21T16:03:00.000-05:00

Research is already under way to defeat death, involving medical scientists and artificial intelligence experts, focusing on creating the technology necessary to upload the brain's contents to a silicon support and then download it again into a new body. This is not science fiction.

42667.jpegIn his article "How to become immortal - upload your mind", US based researcher Terrence Aym* presents the latest focus of the scientific community in achieving immortality.

He claims that the thoughts of futurists, cybernetic experts and artificial intelligence researchers "are converging on the same basic idea: Why not upload everything that's in the brain-everything that makes a person who they are-into a computer and then download it again into a new body? Doing such a thing would make the individual theoretically immortal".

According to his research, there is already a taskforce working on this death-defying project, namely an organization called The Digital Immortality Institute (DII) which "has determined the three things necessary to achieve digital immortality are: guaranteed Internet access; insure the identity integrity of the avatars for each individual user; and finally, make sure the personality, memory, everything that makes up the person as a unique individual, has been uploaded into the digital facsimile before the actual person dies".

What then happens is that "an individual is uploaded into a digital avatar and survives 24/7 within a permanent, theoretically eternal, Internet".

Fantasy? Not quite. The British futurist Ian Pearson, quoted by Terrence Aym, claims that "death will be a thing of the past by 2050". Until then, super computers with massive memory capacity will have been developed (studies indicate that this will take place already by 2020).

Ian Pearson and Anders Sandberg, a member of the transhuman movement, believe that the technology allowing the uploading and downloading of minds is imminent.

Blu-Ray Review: Cronos -- Criterion Collection

2010-12-18T14:36:00.002-05:00

Guillermo del Toro's remastered directorial debut comes to Criterion on Blu-ray.

As a species, people have a fascination with eternal life. The idea of being young and living forever is one that's very popular, spanning across cultures, race, age, and religious backgrounds. Maybe it's the fear of the unknown that does it (what happens to us when we die?) or maybe it's because people love living life and never want it to end. And maybe that's why 1993's Cronos, celebrated filmmaker Guillermo del Toro's directorial debut, strikes such a chord with viewers. It's a film that's accessible to just about anybody as it deals with the appeal of immortality, but also explores the harsh realities that immortal life entails. Getting slapped with an all-new Criterion treatment, Cronos is finally getting the respect it deserves as a fairy tale / horror flick that takes the romance with immortality in a completely different direction.

Jesus Gris (Federico Lupi) comes across a mysterious golden object in his antique store. The object, later to be known as the Cronos, was invented by an alchemist in the 1500s, granting eternal life to anyone who uses it. Unaware of what it is and what it does, Jesus uses the device and immediately begins feeling younger, better, and full of energy ... but at what cost? Dieter de la Guardia is a rich and dying man seeking the Cronos to prolong his ending life, using his thuggish nephew (Ron Perlman) to investigate and instructing him to obtain the Cronos by any means necessary. When the two worlds collide and the awful truth of the Cronos is revealed it's a fight for eternal life ... and for normalcy.

In 1993 Guillermo del Toro wasn't a household name nor was he a name at all: he was just a guy wanting to make a movie. And yet he was at the top of his game with Cronos, a film that echoes many themes and a visual style that del Toro has explored over the last 15 years. His biggest success (at least critically) has been Pan's Labyrinth, released in 2006. If you could pair any two movies together, they'd be Cronos and Pan's Labyrinth, both of which are grim fairy tales told through beautiful visuals with children as the protagonists, and both offer a look at the often frightening consequences of what happens when said fairy tales become a reality. While you couldn't label either film as childish, the films are presented with a sense of child-like awe and wonder that del Toro has the ingenious knack for presenting.

This is the first Criterion release of Cronos and they don't disappoint, offering consumers a restored digital transfer (both audio and video); two separate audio commentary tracks, one by del Toro, the other by the film's director of photography; brand-new video interviews with del Toro, the great Ron Perlman, and actor Federico Luppi; a video tour of del Toro's "man cave" entitled "Welcome to Bleak House," which is a fun little featurette, especially if you're a fan of del Toro, collectibles, and knick-knacks; del Toro's (previously unreleased) short horror film Geometria from 1987; plus a stills and trailer gallery. And if that weren't enough, the disc also comes with a fascinating booklet featuring artwork by Mike Mignola; an essay by film critic Maitland McDonagh; and Director's Notes, which detail the background stories of each of the main characters in the film with parts crossed out and rewritten in del Toro's own handwriting.

If you've ever wondered what kind of films del Toro made before he did Blade II and Hellboy, then look no further than Cronos. The Criterion release is packed full of extras, providing just the right amount of special features to give you a better understanding of the film and of del Toro himself, without being too overbearing or pretentious. If subtle horror is your game or you're a big fan of del Toro's work, then pick up this edition of Cronos.

Live forever no matter what the costs with Cronos, now available on Blu-ray from the Criterion Collection.

Distributed biological computation imitates logic-gate circuits

2010-12-15T18:23:00.000-05:00

Genetically modified yeast cells can be made to communicate with each other as if they were electronic logic circuits, researchers at the University of Gothenburg, Sweden have found.
“Even though engineered cells can’t do the same job as a real computer, our study paves the way for building complex constructions from these cells,” says Kentaro Furukawa at the University of Gothenburg’s Department of Cell- and Molecular Biology, one of the researchers behind the study.
“In the future we expect that it will be possible to use similar cell-to-cell communication systems in the human body to detect changes in the state of health, to help fight illness at an early stage, or to act as biosensors to detect pollutants in connection with our ability to break down toxic substances in the environment.”
Using a library of genetically modified yeast cells, the research team at the University of Gothenburg has produced synthetic circuits based on gene-regulated communication between cells. The yeast cells sense their surroundings and send signals to other yeast cells by secreting molecules. The various types of cells can be combined like Lego bricks to produce more complex circuits, such as a multiplexer or a 1-bit adder with carry. The basic two-input and one-output engineered functions include AND and inverted IMPLIES, which allow for implementing any Boolean function. Using a construction of yeast cells with different genetic modifications, it is possible to carry out more complex computational functions.
Ref.: Distributed biological computation with multicellular engineered networks, Nature, Dec. 8, 2010
Adapted from materials provided by the University of Gothenburg

Cryonic Freezing a Bad Idea?

2010-11-08T19:50:00.000-05:00

Today there was a post on the i09 blog about a Twilight Zone comic book with a story line on Cryonic freezing and why its a bad idea. I thought it was kinda funny. Maybe you will also. Just for the record though I signed up for cryonic freezing with ALCOR 2 years ago. I think of it along the lines of an insurance policy.

You can check out the rest of the comic book story at the i09 blog

Brooke Greenberg: The Eternally Young Toddler

2010-11-07T17:15:00.001-05:00

You may have read this story before when it first hit the news back in 2001 years ago on Dateline and I have written about it in the past but I think this situation deserves special attention.

If you are not familiar with her she is an amazing 17 year old child from Maryland, with the body and mental capabilities of a 1 year old. For all scientists can tell she hasn't aged a day past the age of one. She has had several medical emergencies that have disappeared as quickly as they have appeared.

There has been no diagnosis of any known genetic syndrome or chromosomal abnormalities. Her parents have tried hormonal therapy which did nothing. Shortly after doctors gave her condition a name called Syndrome X.

When geneticists sequenced Greenberg's DNA, they found that the genes associated with the premature aging diseases were normal, unlike the mutated versions in patients with Werner syndrome and progeria.

In 2006, Richard Walker, PhD in endocrine physiology of the University of South Florida College of Medicine, said that Brooke's body is not developing as a coordinated unit, but as independent parts that are out of sync.She has never been diagnosed with any known genetic disorder or chromosomal abnormality that would help explain why.Her telomeres seem to be shortening at the normal rate.

In 2009, Walker said: "There've been very minimal changes in Brooke's brain ... Various parts of her body, rather than all being at the same stage, seem to be disconnected." Walker noted that Greenberg's brain, for example, is not much more mature than that of a newborn infant. He estimates her mental age at around 9 months to a year old. Brooke can make gestures and recognize sounds, but cannot speak. Her bones are like those of a ten-year-old, and she still has her baby teeth, which have an estimated developmental age of about 8 years. Said Walker, "We think that Brooke's condition presents us with a unique opportunity to understand the process of aging."

By 2010 at least two other individuals have been identified with similar developmental issues as Brooke Greenberg.

Walker has an unusual theory about aging which he wants to confirm with data from Brooke. "Aging happens when developmental genes merely run out of meaningful information and subsequently cause chaos," he argues. What if master developmental genes could be shut down?

She has no hormonal problems, and her chromosomes seem normal. But her development is proceeding "extremely slowly," says Walker. If scientists can figure out what is causing the disorder, it might be possible to unlock the mysteries of aging itself. "Then we've got the golden ring," says Walker.

He hopes to simply eliminate age-related diseases like cancer, dementia and diabetes. People who no longer age will no longer get sick, he reasons. But he also thinks eternal life is conceivable. "Biological immortality is possible," says Walker. "If you don't get hit by a car or by lightning, you could live at least 1,000 years."

Aubrey de Grey, a British biologist, argues that the Brooke Greenberg case "has absolutely nothing to do with aging." He favors the standard theory that a body's cells simply wear out over the years.

Resources:
1) Richard Walker
2)Aubrey de Grey

Nanobot replacing a neuron in 3D(HD)

2010-10-31T21:03:00.000-04:00

I just found this cool site of a Neuro-prosthetic nanorobot at work replacing a human neuron with an artificial neuron.
This CG animation visualizes one of the possible future applications and uses of nanotechnology.

Check out the 3d animation version of this --->here<----

Endometrial stem cells could repair brain cells damaged by Parkinson's disease

2010-05-08T16:32:00.000-04:00

LEFT: These are neurons developed from human endometrial stem cells. Credit: Hugh S. Taylor, M.D., Yale University School of Medicine

Stem cells derived from the endometrium (uterine lining) and transplanted into the brains of laboratory mice with Parkinson's disease appear to restore functioning of brain cells damaged by the disease, according to a new study by Yale School of Medicine researchers.

The findings are published in the Journal of Cellular and Molecular Medicine. Although these are preliminary results, the findings increase the likelihood that endometrial tissue could be harvested from women with Parkinson's disease and used to re-grow brain areas that have been damaged by the disease, according to lead author Hugh S. Taylor, M.D., professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale School of Medicine, and section chief of Reproductive Endocrinology and Infertility at Yale School of Medicine.

Because of their ability to divide into new cell types, stem cells could be the key to treating many different kinds of diseases, like Parkinson's, in which the body's own cells are damaged or depleted. Parkinson's is caused by a breakdown of dopamine-producing nerve cells in the brain stem. Dopamine is a neurotransmitter that stimulates the motor neurons that in turn control muscles. When dopamine production is reduced, the nerves are not able to control movement or maintain coordination.
In their study, Taylor and his colleagues collected and cultured endometrial tissue from nine women, and verified that they could be transformed into dopamine-producing nerve cells like those in the brain.
"The dopamine levels in the mice increased once we transferred the endometrial stem cells into their brains," said Taylor. "This is encouraging because women have a ready supply of stem cells that are easily obtained, can differentiate into other cell types. They may have great potential for treating multiple diseases."
Highlighting the benefits of using endometrial stem cells, Taylor said the ethical concerns surrounding the use of embryonic stem cells are eliminated when using adult stem cells. Taylor also points out that endometrial stem cells are one of the best sources for generating neurons because they appear to be less likely to be rejected than stem cells from other sources.
"This is just the tip of the iceberg of what we will be able to do with these cells," said Taylor. "We believe these neurons are only the first of many cell types derived from endometrium that will be used to treat a variety of diseases."

Provided by Yale University (news : web)

Pentagon: Zombie Pigs First, Then Hibernating Soldiers

2009-12-13T06:50:00.001-05:00

Around half of U.S. troop fatalities are caused by blood loss from battlefield injuries. Now, with another 30,000 troops deploying to Afghanistan, the Pentagon is pushing for medical advances that can save more lives during combat. The Defense Department’s latest research idea: Stop bleeding injuries by turning pigs into the semi-undead. If it works out, we humans could be the next ones to be zombified.

Military’s mad-science arm Darpa has awarded $9.9 million to the Texas A&M Institute for Preclinical Studies (TIPS), to develop treatments that can extend a “golden period” when injured war fighters have the best chance of coming back from massive blood loss. Odds of survival plummet after an hour — during combat, that kind of quick evacuation, triage and treatment is often impossible.

The institute’s research will be based on previous Darpa-funded efforts. One project, at Stanford University, hypothesized that humans could one day mimic the hibernation abilities of squirrels — who emerge from winter months no worse for wear — using a pancreatic enzyme we have in common with the critters. The other, led by Dr. Mark Roth at the Fred Hutchinson Cancer Research Center, used nematode worms and rats to test how hydrogen sulfide could block the body’s ability to use oxygen — creating a kind of “suspended animation” where hearts stop beating and wounds don’t bleed. After removing 60 percent of the rat’s blood, Dr. Roth managed to keep the critters alive for 10 hours using his hydrogen sulfide cocktail.

The next logical step: Try the same thing on pigs. They’ve got a similar cardiovascular system to humans, and TIPS researchers Theresa Fossum and Matthew Miller think they can accurately predict human results from the swine trials. Using anesthetized pigs, the doctors are testing various compounds, some containing hydrogen sulfide, to find one that can safely keep the hemorrhaging animals “as close to death as possible.”

With a 15-person team working exclusively on the project, the institute anticipates successful results within 18 months. “Darpa wants this to happen yesterday, because it was needed yesterday,” Dr. Miller told Danger Room. Once the team comes up with the right elixir, it’ll undergo federally mandated safety testing. After that, the zombie vaccine will be sent to the battlefield for human application.

Dr. Fossum predicts that each soldier will carry a syringe into combat zones or remote areas, and medic teams will be equipped with several. A single injection will minimize metabolic needs, de-animating injured troops by shutting down brain and heart function. Once treatment can be carried out, they’ll be “re-animated” and — hopefully — as good as new.

From rats, to pigs, to troops — to civilians. Dr. Miller anticipates dozens of medical applications, including the preservation of organs before transplants and suspension of life-threatening emergencies, like heart attacks and strokes. “Everybody’s talking about the military use of this, and that’s our focus now,” he says. “But really, this could be much, much bigger than that.”

Original article from Wired

Ray Kurzweil on How to Combat Aging

2009-10-14T19:27:00.001-04:00

The noted futurist says that exponential advances will allow us to intervene in the aging process.

Submitted in response to Technology Review's interview with Leonard Hayflick. See "Can Aging Be Solved?"

Entropy is not the most fruitful perspective from which to view aging. There are varying error rates in biological information processes depending on the cell type, and this is part of biology's paradigm. We have means already of determining error-free DNA sequences even though specific cells will contain DNA errors, and we will be in a position to correct those errors that matter.

The most important perspective in my view is that health, medicine, and biology is now an information technology, whereas it used to be hit or miss. We not only have the (outdated) software that biology runs on (our genome), but we have the means of changing that software (our genes) in a mature individual with such technologies as RNA interference and new forms of gene therapy that do not trigger the immune system. (I am a collaborator with a company that performs gene therapy outside the body, replicates the modified cell a million-fold, and reintroduces the cells to the body, a process that has cured a fatal disease--pulmonary hypertension--and is undergoing human trials.)

We can design interventions on computers and test them out on increasingly sophisticated biological simulators. One of my primary themes is that information technology grows exponentially, in sharp contrast to the linear growth of hit or miss approaches that have characterized medicine up until recently. As such, these technologies will be a million times more powerful in 20 years (by doubling in power and price performance each year). The genome project, incidentally, followed exactly this trajectory.

Hayflick cites the automobile as an example to support his thesis that you cannot stop aging. Yes, automobiles will wear out if you don't maintain them adequately. However, we do have the knowledge to perfectly maintain automobiles and completely prevent aging. There are century-old automobiles around in vintage (perfect) condition that are still driven around. That is because the maintenance was sufficiently aggressive for those cars. Most people don't think it's worth the trouble with regard to an automobile, but it will be worth the trouble for our bodies. With regard to automobiles, we have all of the knowledge and tools needed to completely stop aging. We do not yet have all of the knowledge and tools to do this with the human body, but that knowledge is growing exponentially.

As for the implications of radical life extension, Hayflick assumes that nothing else would change. But the same technologies that will bring radical life extension will also bring radical expansion of resources (nanoengineered solar panels, water and food technologies) and radical life expansion (merging with the intelligent machines that we are creating, virtual reality from within the nervous system, etc.). We have already democratized the tools of creativity so that kids in their dorm room can create a full-length high-definition motion picture or write software that results in disruptive change (e.g., Google). Hayflick has not considered the implications of these recent developments. We don't have to do any of these things perfectly (and there is no such thing as perfection in the real world)--just well enough to stay ahead of the curve.

Our intuition is linear, so many scientists, such as Hayflick, think in linear terms and expect that the slow pace of the past will characterize the future. But the reality of progress in information technology is exponential, not linear. My cell phone is a billion times more powerful per dollar than the computer we all shared when I was an undergrad at MIT. And we will do it again in 25 years. What used to take up a building now fits in my pocket, and what now fits in my pocket will fit inside a blood cell in 25 years.

With regard to Hayflick's own limit, he acts as if that limit is impossible to engineer. Just in recent years we have discovered that just one enzyme controls the telomeres and that cancer cells use telomerase to become immortal. Now, I realize that it is not a simple matter to just apply telomerase to overcome this particular aging limit, as we have to figure out how to administer it, and we don't want to encourage cancer, but these are all solvable engineering problems.

Original article by Ray Kurzweil for MIT tech review

Learning to juggle grows brain networks for good

2009-10-13T17:31:00.002-04:00

Juggling boosts the connections between different parts of the brain by tweaking the architecture of the brain's "white matter" – a finding that could lead to new therapies for people with brain injuries.

White matter describes all areas of the brain that contain mostly axons – outgrowths of nerve cells that connect different cells. It might be expected that learning a new, complex task such as juggling should strengthen these connections, but previous work looking for changes in the brains of people who had learned how to juggle had only studied increases in grey matter, which contains the nerve cells' bodies.

Now Jan Scholz and his colleagues at the University of Oxford have discovered that juggling changes white matter, too. They gave 24 young men and women training packs for juggling and had them practise for half an hour a day for six weeks. Before and after this training period, the researchers scanned the brains of the jugglers along with those of 24 people who didn't do any juggling, using a technique called diffusion tensor imaging that reveals the structure of white matter.

They found that there was no change in the brains of the non-jugglers, but the jugglers grew more white matter in a part of the parietal lobe – an area involved in connecting what we see to how we move.

The same transformation was seen in all the jugglers, regardless of how well they could perform. This suggests that it's the learning process itself that is important for brain development, not how good you are.
Learning matters

Arne May of the University Medical Centre Hamburg-Eppendorf in Germany, who led the previous work on juggling and grey matter, finds this result "fascinating". "It suggests that learning a skill is more important than exercising what you are good at already – the brain wants to be puzzled and learn something new," he says.

Like May, Scholz's group found increases in grey matter, but differences in the size and timing of the grey- and white-matter changes suggest they are independent. Nevertheless, both are probably necessary to learn how to juggle, argues Scholz.

"More white matter on its own might mean you can move more quickly, but you'd need the grey matter to make sure your hands were in the right place," he says.
Don't use it, don't lose it

The group scanned the jugglers' brains again after four weeks without juggling. They found that the new white matter had stayed put and the amount of grey matter had even increased. This could be why, when we learn a new skill, we retain some ability, no matter how long ago we last practised.

"It's like riding a bike," Scholz says. "Either you can juggle or you can't. It takes a lot of training to learn, but once it clicks, you don't forget it."

Scholz also hopes that it might be possible to develop juggling-based training programmes to help people with brain injuries, or that further study of how juggling changes the architecture of the brain may lead to the discovery of drugs that could boost this plasticity. "If we could use training or drugs to help stroke patients regenerate damaged parts of their brains, that would be fantastic," he says.

Journal reference: Nature Neuroscience, DOI: 10.1038/nn.2412

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ORIGINAL ARTICLE by Jessica Hamzelou for new scientist

First Drug Shown to Extend Life Span in Mammals

2009-10-10T20:27:00.003-04:00

Rapamycin, an immunosuppressant, enables elderly mice to live longer.

A drug derived from bacteria in the soil on Easter Island can substantially extend the life span of mice, according to a study published online today in Nature. The drug, called rapamycin, is the first pharmacological agent shown to enhance longevity in a mammal, and it works when administered beginning late in life. Prior to this research, the only ways to increase rodents' life span were via genetic engineering or caloric restriction--a nutritionally complete but very low-calorie diet.

Rapamycin is an antifungal compound already approved by the FDA as an immunosuppressive therapy to help prevent organ rejection in transplant patients. It is currently being tested in clinical trials for potential anticancer effects.

The drug had previously been shown to extend life span in invertebrates. "[This study is] exciting because it shows that it's feasible to do this in a mammal," says David Sinclair, codirector of the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging at Harvard Medical School, who was not involved in the study. "Maybe 20 years from now we'll look back at this study as a landmark that pointed the way to medicines of the future."

In the new study, researchers found that rapamycin given to mice as a food supplement starting at 20 months of age--the equivalent of 60 years in humans--extended average life span by 9 percent in males and 13 percent in females. "It's particularly exciting because it works so late in life to extend life span," says Sinclair. "The fact that you can give a drug after 20 months of age in a mouse and still see a life-span extension is striking."

The results were pooled from three independent studies--at Jackson Laboratory, in Bar Harbor, ME; the University of Texas Health Science Center, in San Antonio; and the University of Michigan, in Ann Arbor--and coordinated by the National Institute of Aging's Interventions Testing Program (ITP). Rapamycin is the first success story to emerge from the ITP, which systematically evaluates anti-aging drug candidates for effectiveness in mice.

Experts believe it's possible that rapamycin may tap into one of the same biochemical pathways as calorie restriction, an intervention long known to make mice live longer. While the drug was not as effective as a limited diet initiated early in life, it was far more powerful than a limited diet begun at the same advanced age. In ongoing studies, the researchers are testing different doses across a range of starting ages; an optimal combination may ultimately prove more potent than calorie restriction.

Stumbling across rapamycin's late-in-life efficacy was a happy accident. Originally, the therapy was to begin at four months of age, but the amount of rapamycin required to sustain therapeutic blood levels turned out to be prohibitively expensive. By the time the researchers devised a solution--microencapsulating the drug in a polymer coating that only disintegrates in the intestine--the mice were much older.

The research team decided to go ahead with the study anyway, because if there was an effect with late-in-life administration, it would be particularly relevant for humans. Initiating a human treatment early in life would be less practical, and would expose patients to side effects for longer, says David Harrison, principal investigator of the Jackson Laboratory portion of the study. (Because the drug suppresses the immune system, patients taking it are more susceptible to dangerous infections.)

Besides targeting older animals, the study is also unusual for its use of a genetically diverse population of mice. Most aging studies use inbred strains, which are easier to work with in the laboratory. Harrison says that a genetically heterogeneous study population rules out the possibility of accidentally treating a specific disease that happens to be prevalent in the inbred strain being used. Much like humans, the mice used in the study have a wide variety of susceptibility to the various diseases of aging. Since the life-span-extending effects were seen throughout the study population, says Harrison, rapamycin must be altering some fundamental aging mechanism that drives a broad range of age-related defects.

"People who study the biology of aging feel that in order to deal with diseases of aging, it's much more efficient to target underlying mechanisms, rather than focusing on heart disease or cancer or diabetes or Alzheimer's or Parkinson's separately," says Harrison. "If we could alter underlying mechanisms of aging, all of these things would be postponed."

Exactly what rapamycin's mechanism might be remains to be seen, says Harrison. The drug inhibits a protein called target of rapamycin (TOR). Normally, TOR helps cells manufacture new proteins, and hinders the destruction of malfunctioning ones. While these processes are known to be involved in aging in fruit flies, nematode worms, and yeast, TOR's precise role in life-span regulation is still unclear.

It's promising to learn that TOR also participates in mouse aging, because it means that the mechanism is relevant in all four model organisms most widely used to study the aging process, says Matt Kaeberlein, a professor of pathology at the University of Washington and coauthor of a commentary accompanying the new study. "The fact that it's been conserved over that large evolutionary distance makes it an intriguing possibility that TOR signaling has similar effects in people," he says.

Teasing out precisely how TOR signaling is linked to life span could reveal new targets for potential anti-aging drugs. By zeroing in on a different part of the TOR pathway, future drugs may be able to avoid some of rapamycin's troubling side effects.

The authors caution that it's still not clear whether rapamycin will have similar life-span-enhancing effects in humans, and that because of its known toxicities, such as fungal infections and pneumonia, the drug should not be taken by the general population as a kind of universal fountain of youth.

A more realistic goal, says Kaeberlein, is to investigate whether it can treat specific age-related disorders--as in the several ongoing cancer trials, for example. Studies have also suggested that interfering with the TOR signaling pathway could slow the progression of Huntington's disease, Alzheimer's disease, and diabetes. "Realistically," says Kaeberlein, "I think what most of us are hoping for, and are somewhat optimistic about, is the idea that you may be able to get an extra decade--possibly an extra two decades--of relatively good health."

Original article by Jocelyn Rice for MIT tech review

Brain-wave boost sets us to slow motion

2009-10-08T12:48:00.002-04:00

Boosting brain waves can make people move in slow motion. This finding is one of the first to show that brain waves directly influence behaviour, and it could lead to new treatments for Parkinson's disease and other disorders that affect movement.

Peter Brown and his colleagues at University College London generated a small electrical current in the brains of 14 healthy volunteers using scalp electrodes. The current increased the activity of normal beta waves – a kind of brain wave that is usually active during sustained muscle activities, such as holding a book. Beta activity usually drops before people begin a movement.

The participants then carried out a simple task: they moved a spot on a computer screen as quickly as possible using a joystick. When beta wave activity increased, their fastest times slowed by 10 per cent.

"This is the first time that beta wave activity has been shown to slow movement," Brown says.

Deep currents

Other studies have found that people with Parkinson's disease have greater beta activity. Brown's research suggests this could be linked to the slowing of movement seen in those with the disease. Electrical stimulation deep in the brain is used to treat people with Parkinson's, although how it works is a subject of debate.

The electrical currents used in the new study were too small to be felt by the participants, and the researchers were surprised they had such a measurable effect.

"It's very interesting that artificially boosting the beta wave slows movements," says Stuart Baker of Newcastle University, UK. "This is a completely new way of thinking about how to treat patients with Parkinson's disease."

The findings are even more relevant for conditions of uncontrolled movement, such as dystonia and chorea, Brown said. "An electrode could be inserted under the skull to boost brain activity and slow down uncontrolled movement."

Journal reference: Current Biology, DOI: 10.1016/j.cub.2009.07.074

Original article written for New Scientist by Jessica Hamzelou

Self-Destructive Behavior in Cells May Hold Key to a Longer Life

2009-10-07T12:36:00.002-04:00

Deep down, we are all cannibals. Our cells are perpetually devouring themselves, shredding their own complex molecules to pieces and recycling them for new parts. Many of the details of our endless self-destruction have come to light only in the past few years. And to the surprise of many scientists, links are now emerging between this inner cannibalism and diseases like Alzheimer’s disease and cancer.

Above:Biological Recycling

“There’s been an explosion,” said Daniel Klionsky of the University of Michigan. “All of a sudden researchers in different fields are seeing a connection.”

In fact, as Dr. Klionsky wrote in a paper published online in Trends in Cell Biology, this cannibalism may extend our lifespan. Increasing our body’s ability to self-destruct may, paradoxically, let us live longer.

Our cells build two kinds of recycling factories. One kind, known as the proteasome, is a tiny cluster of proteins. It slurps up individual proteins like a child sucking a piece of spaghetti. Once inside the proteasome, the protein is chopped up into its building blocks.

For bigger demolition jobs, our cells rely on a bigger factory: a giant bubble packed with toxic enzymes, known as a lysosome. Lysosomes can destroy big structures, like mitochondria, the sausage-shaped sacs in cells that generate fuel. To devour a mitochondrion, a cell first swaddles it in a shroudlike membrane, which is then transported to a lysosome. The shroud merges seamlessly into the lysosome, which then rips the mitochondrion apart. Its remains are spit back out through channels on the lysosome’s surface.

Lysosomes are versatile garbage disposals. In addition to taking in shrouded material, they can also pull in individual proteins through special portals on their surface. Lysosomes can even extend a mouthlike projection from their membrane and chew off pieces of a cell.

The shredded debris that streams out of the lysosomes is not useless waste. A cell uses the material to build new molecules, gradually recreating itself from old parts. “Every three days, you basically have a new heart,” said Dr. Ana Maria Cuervo, a molecular biologist at Albert Einstein College of Medicine.

This self-destruction may seem like a reckless waste of time and energy. Yet it is essential for our survival, and in many different ways. Proteasomes destroy certain proteins quickly, allowing them to survive for only about half an hour. That speed allows cells to keep tight control over the concentrations of the proteins. By tweaking the rate of destruction, it can swiftly raise or lower the number of any kind of protein.

Lysosomes, which eat more slowly than proteasomes, serve different roles that are no less essential. They allow cells to continue to build new molecules even when they are not getting a steady supply of raw ingredients from the food we eat. Lysosomes also devour oily droplets and stores of starch, releasing energy that cells can use to power the construction of new molecules.

“If you don’t have a snack between lunch and dinner,” Dr. Cuervo said, “you’re going to have to activate your lysosomes to get nutrients.”

Lysosomes become even more active if dinner never comes, and a short-term hunger turns to long-term starvation. Cells respond to famine by making only a small number of crucial molecules and using lysosomes to destroy the rest. “When times are good, make everything,” Dr. Klionsky said. “When times are lean, focus on what you need. You can get rid of everything else.”

This strategy for survival, known as autophagy (“eating oneself”), evolved in our ancestors over two billion years ago. Today, all animals rely on it to endure famines, as do plants, fungi and single-cell protozoa.

Autophagy’s great antiquity has helped scientists discover the genes that make it possible in humans. Rather than study starving people, they introduced mutations into yeast and then observed which strains could no longer survive without food. In many cases, the scientists discovered, the mutations that made yeast vulnerable struck genes that are involved in autophagy. They were then able to find nearly identical versions of those genes in the human genome.

The protection humans get from lysosomes is essential not just during famines. It is also vital just after birth. When babies emerge from their mothers, they need huge amounts of energy so that they can start to run their bodies on their own. But this demand comes at precisely the moment that babies stop getting food through their umbilical cord. Japanese scientists have found that lysosomes in mice kick into high gear as soon as they are born. After a day or two, as they start to nurse, the rate of autophagy drops back to normal.

When the scientists engineered mice so they could not use their lysosomes at birth, the newborn mice almost immediately died of starvation.

Body Posture Affects Confidence In Your Own Thoughts, Study Finds

2009-10-07T12:31:00.002-04:00

Sitting up straight in your chair isn't just good for your posture – it also gives you more confidence in your own thoughts, according to a new study.

Researchers found that people who were told to sit up straight were more likely to believe thoughts they wrote down while in that posture concerning whether they were qualified for a job.

On the other hand, those who were slumped over their desks were less likely to accept these written-down feelings about their own qualifications.

The results show how our body posture can affect not only what others think about us, but also how we think about ourselves, said Richard Petty, co-author of the study and professor of psychology at Ohio State University.

"Most of us were taught that sitting up straight gives a good impression to other people," Petty said. "But it turns out that our posture can also affect how we think about ourselves. If you sit up straight, you end up convincing yourself by the posture you're in."

Petty conducted the study with Pablo Briñol, a former postdoctoral fellow at Ohio State now at the Universidad Autónoma de Madrid in Spain, and Benjamin Wagner, a current graduate student at Ohio State. The research appears in the October 2009 issue of the European Journal of Social Psychology.

The study included 71 students at Ohio State. When they entered the lab for the experiment, the participants were told they would be taking part in two separate studies at the same time, one organized by the business school and one by the arts school.

They were told the arts study was examining factors contributing to people's acting abilities, in this case, the ability to maintain a specific posture while engaging in other activities. They were seated at a computer terminal and instructed to either "sit up straight" and "push out [their] chest]" or "sit slouched forward" with their "face looking at [their] knees."

While in one of these positions, students participated in the business study, which supposedly investigated factors contributing to job satisfaction and professional performance.

While holding their posture, students listed either three positive or three negative personal traits relating to future professional performance on the job.

After completing this task, the students took a survey in which they rated themselves on how well they would
do as a future professional employee.

The results were striking.

How the students rated themselves as future professionals depended on which posture they held as they wrote the positive or negative traits.

Students who held the upright, confident posture were much more likely to rate themselves in line with the positive or negative traits they wrote down.

In other words, if they wrote positive traits about themselves, they rated themselves more highly, and if they wrote negative traits about themselves, they rated themselves lower.

"Their confident, upright posture gave them more confidence in their own thoughts, whether they were positive or negative," Petty said.

However, students who assumed the slumped over, less confident posture, didn't seem convinced by their own thoughts – their ratings didn't differ much regardless of whether they wrote positive or negative things about themselves.

The end result of this was that when students wrote positive thoughts about themselves, they rated themselves more highly when in the upright than the slouched posture because the upright posture led to confidence in the positive thoughts.

However, when students wrote negative thoughts about themselves, they rated themselves more negatively in
the upright than the slouched posture because the upright posture led to more confidence in their negative thoughts.

Petty emphasized that while students were told to sit up straight or to slump down, the researchers did not use the words "confident" or "doubt" in the instructions or gave any indication about how the posture was supposed to make them feel.

In a separate experiment, the researchers repeated the same scenario with a different group of students, but asked them a series of questions afterwards about how they felt during the course of the study.
"These participants didn't report feeling more confident in the upright position than they did in the slouched position, even though those in the upright position did report more confidence in the thoughts they generated," Petty said.

That suggests people's thoughts are influenced by their posture, even though they don't realize that is what's happening.

"People assume their confidence is coming from their own thoughts. They don't realize their posture is affecting how much they believe in what they're thinking," he said.
"If they did realize that, posture wouldn't have such an effect."

This research extends a 2003 study by Petty and Briñol which found similar results for head nodding. In that case, people had more confidence in thoughts they generated when they nodded their head up and down compared to when they shook their head from side to side.

However, Petty noted that body posture is a static pose compared to head nodding, and probably more natural and easy to use in day-to-day life.

"Sitting up straight is something you can train yourself to do, and it has psychological benefits – as long as you generally have positive thoughts," he said.

For example, students are often told when taking a multiple-choice test that if they're not absolutely sure of the answer, their first best guess is more often correct.

"If a student is sitting up straight, he may be more likely to believe his first answer. But if he is slumped down, he may change it and end up not performing as well on the test," he said.

You can find other solutions to improve your body posture at Amazon here

Adapted from materials provided by Ohio State University.

Mediterranean Diet Associated With Reduced Risk Of Depression

2009-10-06T13:56:00.001-04:00

ScienceDaily (Oct. 6, 2009) — Individuals who follow the Mediterranean dietary pattern—rich in vegetables, fruits, nuts, whole grains and fish—appear less likely to develop depression, according to a report in the October issue of Archives of General Psychiatry, one of the JAMA/Archives journals.

The lifetime prevalence of mental disorders has been found to be lower in Mediterranean than Northern European countries, according to background information in the article. One plausible explanation is that the diet commonly followed in the region may be protective against depression. Previous research has suggested that the monounsaturated fatty acids in olive oil—used abundantly in the Mediterranean diet—may be associated with a lower risk of severe depressive symptoms.

Almudena Sánchez-Villegas, B.Pharm., Ph.D., of University of Las Palmas de Gran Canaria and Clinic of the University of Navarra, Pamplona, Spain, and colleagues studied 10,094 healthy Spanish participants who completed an initial questionnaire between 1999 and 2005. Participants reported their dietary intake on a food frequency questionnaire, and the researchers calculated their adherence to the Mediterranean diet based on nine components (high ratio of monounsaturated fatty acids to saturated fatty acids; moderate intake of alcohol and dairy products; low intake of meat; and high intake of legumes, fruit and nuts, cereals, vegetables and fish).

After a median (midpoint) of 4.4 years of follow-up, 480 new cases of depression were identified, including 156 in men and 324 in women. Individuals who followed the Mediterranean diet most closely had a greater than 30 percent reduction in the risk of depression than whose who had the lowest Mediterranean diet scores. The association did not change when the results were adjusted for other markers of a healthy lifestyle, including marital status and use of seatbelts.

"The specific mechanisms by which a better adherence to the Mediterranean dietary pattern could help to prevent the occurrence of depression are not well known," the authors write. Components of the diet may improve blood vessel function, fight inflammation, reduce risk for heart disease and repair oxygen-related cell damage, all of which may decrease the chances of developing depression.

"However, the role of the overall dietary pattern may be more important than the effect of single components. It is plausible that the synergistic combination of a sufficient provision of omega-three fatty acids together with other natural unsaturated fatty acids and antioxidants from olive oil and nuts, flavonoids and other phytochemicals from fruit and other plant foods and large amounts of natural folates and other B vitamins in the overall Mediterranean dietary pattern may exert a fair degree of protection against depression," the authors write.

Journal reference:

Almudena Sanchez-Villegas; Miguel Delgado-Rodriguez; Alvaro Alonso; Javier Schlatter; Francisca Lahortiga; Lluis Serra Majem; Miguel Angel Martinez-Gonzalez. Association of the Mediterranean Dietary Pattern With the Incidence of Depression: The Seguimiento Universidad de Navarra/University of Navarra Follow-up (SUN) Cohort. Arch Gen Psychiatry, 2009; 66 (10): 1090-1098 [link]

Adapted from materials provided by JAMA and Archives Journals.

New mathematical model may help reverse-engineer the brain

2009-10-04T19:53:00.002-04:00

New model suggests how the brain might stay in balance

The human brain is made up of 100 billion neurons — live wires that must be kept in delicate balance to stabilize the world’s most magnificent computing organ. Too much excitement and the network will slip into an apoplectic, uncomprehending chaos. Too much inhibition and it will flatline. A new mathematical model describes how the trillions of interconnections among neurons could maintain a stable but dynamic relationship that leaves the brain sensitive enough to respond to stimulation without veering into a blind seizure.

Marcelo O. Magnasco, head of the Laboratory of Mathematical Physics at The Rockefeller University, and his colleagues developed the model to address how such a massively complex and responsive network such as the brain can balance the opposing forces of excitation and inhibition. His model’s key assumption: Neurons function together in localized groups to preserve stability. “The defining characteristic of our system is that the unit of behavior is not the individual neuron or a local neural circuit but rather groups of neurons that can oscillate in synchrony,” Magnasco says. “The result is that the system is much more tolerant to faults: Individual neurons may or may not fire, individual connections may or may not transmit information to the next neuron, but the system keeps going.”

Magnasco’s model differs from traditional models of neural networks, which assume that each time a neuron fires and stimulates an adjoining neuron, the strength of the connection between the two increases. This is called the Hebbian theory of synaptic plasticity and is the classical model for learning. “But our system is anti-Hebbian,” Magnasco says. “If the connections among any groups of neurons are strongly oscillating together, they are weakened because they threaten homeostasis. Instead of trying to learn, our neurons are trying to forget.” One advantage of this anti-Hebbian model is that it balances a network with a much larger number of degrees of freedom than classical models can accommodate, a flexibility that is likely required by a computer as complex as the brain.

In work published this summer in Physical Review Letters, Magnasco theorizes that the connections that balance excitation and inhibition are continually flirting with instability. He likens the behavior to an indefinitely large number of public address systems tweaked to that critical point at which a flick of the microphone brings on a screech of feedback that then fades to quiet with time.

This model of a balanced neural network is abstract — it does not try to recreate any specific neural function such as learning. But it requires only half of the network connections to establish the homeostatic balance of exhibition and inhibition crucial to all other brain activity. The other half of the network could be used for other functions that may be compatible with more traditional models of neural networks, including Hebbian learning, Magnasco says.

Developing a systematic theory of how neurons communicate could provide a key to some of the basic questions that researchers are exploring through experiments, Magnasco hopes. “We’re trying to reverse-engineer the brain and clearly there are some concepts we’re missing,” he says. “This model could be one part of a better understanding. It has a large number of interesting properties that make it a suitable substrate for a large-scale computing device.”

Original article by the Rockefeller University

New mathematical model may help reverse-engineer the brain

2009-10-04T19:53:00.001-04:00

New model suggests how the brain might stay in balance

Scientists Develop Nasal Spray That Improves Memory

2009-10-04T19:32:00.002-04:00

Good news for procrastinating students: a nasal spray developed by a team of German scientists promises to give late night cram sessions a major boost, if a good night's sleep follows. (Credit: iStockphoto/Ana Blazic)

ScienceDaily (Oct. 2, 2009) — Good news for procrastinating students: a nasal spray developed by a team of German scientists promises to give late night cram sessions a major boost, if a good night's sleep follows. In a research report featured as the cover story of the October 2009 print issue of The FASEB Journal, these scientists show that a molecule from the body's immune system (interleukin-6) when administered through the nose helps the brain retain emotional and procedural memories during REM sleep.

"Sleep to remember, a dream or reality?" said Lisa Marshall, co-author of the study, from the Department of Neuroendocrinology at the University of Lubeck in Germany. "Here, we provide the first evidence that the immunoregulatory signal interleukin-6 plays a beneficial role in sleep-dependent formation of long-term memory in humans."

To make this discovery, Marshall and colleagues had 17 healthy young men spend two nights in the laboratory. On each night after reading either an emotional or neutral short story, they sprayed a fluid into their nostrils which contained either interleukin-6 or a placebo fluid. The subsequent sleep and brain electric activity was monitored throughout the night. The next morning subjects wrote down as many words as they could remember from each of the two stories. Those who received the dose of IL-6 could remember more words.

"If a nasal spray can improve memory, perhaps we're on our way to giving some folks a whiff of common sense, such as accepting the realities of evolution," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This is exciting piece of interdisciplinary science, since IL-6 had previously been considered a by-product of inflammation, not an agent that affects cognition."

Journal reference:

Christian Benedict, Jürgen Scheller, Stefan Rose-John, Jan Born, and Lisa Marshall. Enhancing influence of intranasal interleukin-6 on slow-wave activity and memory consolidation during sleep. FASEB J., 2009 23: 3629-3636 DOI: 10.1096/fj.08-122853

Adapted from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS.

A Genetic Fountain of Youth

2009-10-03T19:24:00.002-04:00

Aging machines: Mice lacking a functional version of the protein S6 kinase 1, an important regulator of the body's response to nutrient availability, live longer and healthier lives than their normal counterparts. The mouse on the left lacks the protein.Researchers have identified a genetic tweak that can slow aging in mice.

By disabling a gene involved in an important biochemical signaling pathway, scientists have discovered a way to mimic the well-known anti-aging benefits of caloric restriction, allowing mice to live longer and healthier lives. This finding, published online today in Science, offers a promising drug target for combating the many health problems associated with aging.

"This research points the way to potential pharmacological approaches to treating aging-related diseases in humans," says senior author Dominic Withers, professor of diabetes and endocrinology at University College London.

"It really defines this as a pathway that's affecting aging all the way from yeast to mammals, which I think is pretty striking," says Matt Kaeberlein, professor of pathology at the University of Washington and coauthor of a commentary accompanying the new study.

Caloric restriction has long been known to extend lifespan and reduce the incidence of age-related diseases in a wide variety of organisms, from yeast and roundworms to rodents and primates. Exactly how a nutritionally complete but radically restricted diet achieves these benefits has remained unclear. But recently several studies have offered evidence that a particular signaling pathway, involving a protein called target of rapamycin (TOR), may play a pivotal role. This pathway acts as a sort of food sensor, helping to regulate the body's metabolic response to nutrient availability.

Withers and colleagues noticed that young mice with a disabled version of the protein S6 kinase 1 (S6K1), which is directly activated by TOR, bore strong resemblance to calorie-restricted mice: they were leaner and had greater insulin sensitivity than normal mice. The researchers wondered whether these benefits would persist into middle and late age, and whether the mice

To find out, they bred two large groups of "knockout" mice that lacked a functional version of the gene for S6K1. One group lived out their lives undisturbed, providing a measure of the group's natural lifespan. The other group was put through extensive testing of cognitive and motor performance and metabolic health.

In female mice, the results were profound. Knockout females lived substantially longer than their normal counterparts. At 600 days--the mouse equivalent of human middle age--they excelled at motor performance tests, outdoing normal mice at tasks requiring balance, strength, and coordination. They were also more inquisitive and apt to explore new environments, suggesting improved cognitive function. Physiological measures also pointed to better health: the knockout mice had stronger bones, better insulin sensitivity, and more robust immune cells. While male knockout mice did not have extended lifespans, they did have the same array of health benefits as females.

To read the rest or the original article go to MIT TEch Review

Quest for a Long Life Gains Scientific Respect

2009-10-02T08:26:00.002-04:00

BOSTON — Who would have thought it? The quest for eternal life, or at least prolonged youthfulness, has now migrated from the outer fringes of alternative medicine to the halls of Harvard Medical School.

AGE WELL David Sinclair, left, and Christoph Westphal, co-founders of Sitris Pharmaceuticals, in Dr. Sinclair’s laboratory in Cambrdge, Mass. The company develops drugs that mimic resveratrol, a chemical found in some red wines.

At a conference on aging held here last week, the medical school’s dean, Jeffrey Flier, was to be seen greeting participants who ranged from members of the 120 club (they intend to live at least that long) to devotees of very low calorie diets.

The heavyweight at the conference was Sirtris Pharmaceuticals. The company is developing drugs that mimic resveratrol, a chemical found in some red wines. Resveratrol has been found to activate proteins called sirtuins, from which the company derives its name. Activation of sirtuins is thought to help the body ride out famines.

Mice and rats put on a diet with 30 percent fewer calories can live up to 40 percent longer. They seem to do so by avoiding the usual degenerative diseases of aging and so gain not just longer life but more time in good health.

Sirtris’s researchers think that drugs that activate sirtuins mimic this process, strengthening the body’s resistance to the diseases of aging. The company has developed thousands of small chemical compounds that are far more potent than resveratrol and so can be given in smaller doses.

In mice, sirtuin activators are effective against lung and colon cancer, melanoma, lymphoma, Type 2 diabetes, cardiovascular disease and Alzheimer’s disease, said David Sinclair, a Harvard Medical School researcher and co-founder of Sirtris. The drugs reduce inflammation, and if they have the same effects in people, could help combat many diseases that have an inflammatory component, like irritable bowel syndrome and glaucoma.

Any sirtuin activator that averted all these diseases in people would be a rather remarkable drug. So there is considerable interest in how well Sirtris’s drug trials are going.

Sirtris’s senior director of corporate development, Brian Gallagher, said at the conference that four active clinical trials were under way.

SRT-501, the company’s special formulation of resveratrol, is being tested against two cancers, multiple myeloma and colon cancer that has spread to the liver. A chemical mimic of resveratrol, known as SRT-2104, is in a Phase 2 trial for Type 2 diabetes, and in a Phase 1 trial in elderly patients. (Phase 1 trials test for safety, Phase 2 for efficacy.)

Dr. Gallagher said that unpublished tests in mice showed that another chemical mimic, SRT-1720, increased both health and lifespan; after two years, twice as many mice taking the drug were alive compared with the undosed animals. Resveratrol itself has not been shown to increase lifespan in normal mice, although it does so in obese mice, laboratory roundworms and flies.

Sirtris has so far been doubly fortunate. No severe side effects have yet emerged from the clinical trials. The company has also been lucky in having apparently picked the right horse, or at least a good one, in a fast-developing field.

Besides the sirtuins, several other proteins are now known to influence longevity, energy use and the response to caloric restriction. These include the receptors for insulin and for another hormone called IGF-1, and a protein of increasing interest called TOR (“target of rapamycin”). Rapamycin is an antimicrobial that was recently found to extend lifespan significantly, even when given to mice at an advanced age. Since TOR is involved in the response to caloric restriction, rapamycin may extend life through this pathway.

Sirtuins may not be the most important genes for longevity, Dr. Sinclair conceded at the conference, because the pathways controlled by the sirtuins, TOR and the others “all talk to each other, often by feedback loops.”

Many theories of aging attribute senescence to the inexorable buildup of mutations in a person’s DNA. Dr. Sinclair said that in his view “aging can be reversed” because the DNA mutations did not directly cause aging. Rather, they induce the sirtuin molecules that help control the genome to divert to the site of damage. With the sirtuins absent from their usual post, genes are not regulated efficiently, and the cells’ performance degrades. Diversion of the sirtuins should be a reversible process, in Dr. Sinclair’s view, unlike DNA damage, which is not.

“In five or six or seven years,” said Christoph Westphal, Sirtris’s other co-founder, “there will be drugs that prolong longevity.”

But neither Dr. Sinclair nor Dr. Westphal was the most optimistic person at the conference. That status belonged to the English gerontologist Aubrey de Grey, who sports a beard so luxuriant that it is hard to see if he is wearing a tie. His goal is “negligible senescence.”

Some attendees were so convinced of the virtues of less food that they have begun severe diets of various kinds. Cynthia Kenyon, of the University of California, San Francisco, said she had gone on a low-carb diet in 2002 after finding that food with even 2 percent sugar reduced the lifespan of the laboratory roundworms she studies. “Basically I try to steer clear of desserts and starches, though I do eat chocolate,” she said.

Her willowy figure makes her look at least a decade younger than her age. But a practitioner of more severe caloric restriction who was at the conference looked gaunt and a little frail.

Sirtris’s quest for longevity drugs is founded on solid and promising research. But most drugs fail at some stage during trials. So there is no guarantee that any of Sirtris’s candidate compounds will work in people. The first result from a Phase 2 clinical trial is not expected until the end of next year at the earliest.

Meanwhile, it is a pleasant and not wholly unfounded thought that, just possibly, a single drug might combat every degenerative disease of Western civilization.

oRIGINAL ARTICLE BY nICHOLAS wADE FOR THE nEW yORK tIMES

Protein inhibitor helps rid brain of toxic tau protein

2009-10-01T12:55:00.002-04:00

The University of South Florida team led by neuroscientist Chad Dickey, Ph.D., studies how to manipulate with drugs or gene therapy the proteins that control tau's fate. Credit: University of South Florida

Inhibiting the protein Hsp70 rapidly reduces brain levels of tau, a protein associated with Alzheimer's disease when it builds up abnormally inside nerve cells affecting memory, neuroscientists at the University of South Florida found. The study is reported online today in the Journal of Neuroscience.

"Now that we've discovered that targeting the chaperone protein Hsp70 can clear tau, it could be helpful in finding more effective drugs for Alzheimer's disease," said the study's senior author Chad Dickey, PhD, assistant professor of molecular medicine who works out of the Byrd Alzheimer's Institute at USF Health "The therapeutic strategy may also be applicable to other neurodegenerative diseases involving Hsp70, such as Huntington disease, amyotrophic lateral sclerosis (ALS), and some cancers."

Hsp70 is a one of several "chaperone" proteins that supervises the activity of tau inside nerve cells. The normal function of tau is to support the structure of nerve cells, much like the skeleton provides a scaffold to support the body. Tau is inside nerve cells, while another hallmark protein associated with Alzheimer's, beta amyloid, is outside the neurons.

Working with researchers at the University of Michigan, the USF team tested the effects of several compounds on Hsp70 in cell models and brain tissue from mice genetically modified to develop the memory-choking tau tangles. Some compounds activated Hsp70, and others were Hsp70-inhibitors.

One of the more effective Hsp70-inhibitor drugs the researchers discovered was a derivative of methylthioninium chloride, or Rember™, the first experimental medication reported to directly attack the tau tangles in patients with Alzheimer's disease. Rember was heralded as a major development in the fight against Alzheimer's when results in early clinical trials were announced last year at the International Conference on Alzheimer's disease.

But Rember and its derivatives do have some inherent problems; they're not very potent so effective therapy would require fairly high doses, Dickey said.

"The drug does help prevent the protein (tau) from clumping together, but that in itself doesn't mean it's actively getting rid of the toxic tau," he said. "Now that we know Hsp70 is a target of Rember, we can develop similarly-acting drugs that will more specifically target this chaperone protein in affected areas of the brain, resulting in fewer side effects."

The USF researchers originally thought activating Hsp70 would direct the chaperone protein to decrease the tau gone bad -- preventing tau from stacking up into tangles inside cells involved in memory and destroying them. But instead of restoring tau to its normal supportive function, activating Hsp70 actually led to tau's preservation and even more accumulation, Dickey said. "Basically we think the chaperone binds to the tau, and somehow in the process of trying to fix things decides to keep holding onto tau when it shouldn't. So, activating Hsp70 is not necessarily what we want to do; we ultimately want to inhibit Hsp70 to promote the release or clearance of tau …to kill the bad tau."

Dr. Dickey emphasizes that problems with Hsp70 alone do not cause Alzheimer's. It likely develops from a convergence of various factors in the brain, he said, including deposits of the other featured Alzheimer's protein beta amyloid, or a genetic defect; disruption of cell signaling; a breakdown in the neuron's support structure, and then accumulation of tau into the memory-choking tangles.

Dr. Dickey's team at USF focuses on how to manipulate with drugs or gene therapy the chaperone proteins that regulate tau's fate - determining whether it's preserved or cleared from the brain. The University of Michigan team works on identifying and developing compounds that may be effective against Alzheimer's disease and other tauopathies.

Source: University of South Florida

By 2040 you will be able to upload your brain,,,

2009-09-28T14:29:00.002-04:00

Standing up for GM: Kurzweil believes that opposition to advances such as genetic modification harm humankind

...or at least that's what Ray Kurzweil thinks. He has spent his life inventing machines that help people, from the blind to dyslexics. Now, he believes we're on the brink of a new age – the 'singularity' – when mind-boggling technology will allow us to email each other toast, run as fast as Usain Bolt (for 15 minutes) – and even live forever. Is there sense to his science – or is the man who reasons that one day he'll bring his dad back from the grave just a mad professor peddling a nightmare vision of the future?

Should, by some terrible misfortune, Ray Kurzweil shuffle off his mortal coil tomorrow, the obituaries would record an inventor of rare and visionary talent. In 1976, he created the first machine capable of reading books to the blind, and less than a decade later he built the K250: the first music synthesizer to nigh-on perfectly duplicate the sound of a grand piano. His Kurzweil 3000 educational software, which helps students with learning difficulties such as dyslexia and attention deficit disorder, is likewise typical of an innovator who has made his name by combining restless imagination with technological ingenuity and a commendable sense of social responsibility.

However, these past accomplishments, as impressive as they are, would tell only half the Kurzweil story. The rest of his biography – the essence of his very existence, he would contend – belongs to the future.

Following the publication of his 2005 book, The Singularity is Near: When Humans Transcend Biology, Kurzweil has become known, above all, as a technology speculator whose predictions have polarised opinion – from stone-cold scepticism and splenetic disagreement to dedicated hero worship and admiration. It's not just that he boldly envisions a tomorrow's world where, for example, tiny robots will reverse the effects of pollution, artificial intelligence will far outstrip (and supplement) biological human intelligence, and humankind "will be able to live indefinitely without ageing". No, the real reason Kurzweil has become such a magnet for blogospheric debate, and a tech-celebrity, is that he's convinced those future predictions – and many more just as stunning – are imminent occurrences. They will all, he steadfastly maintains, happen before the middle of the 21st century.

Which means, regarding the earlier allusion to his mortal coil, that he doesn't plan to do any shuffling any time soon. Ray Kurzweil, 61, sincerely believes that his own immortality is a realistic proposition... and just as strongly contends that, using a combination of grave-site DNA and future technologies, he will be able to reclaim his father, Fredric Kurzweil (the victim of a fatal heart attack in 1970), from death.

Just when will this ultimate life-affirming feat be possible? In Kurzweil's estimation, we will be able to upload the human brain to a computer, capturing "a person's entire personality, memory, skills and history", by the end of the 2030s; humans and non-biological machines will then merge so effectively that the differences between them will no longer matter; and, after that, human intelligence, transformed for the better, will start to expand outward into the universe, around about 2045. With this last prediction, Kurzweil is referring not to any recognisable type of space travel, but to a kind of space infusion. "Intelligence," he writes, "will begin to saturate the matter and energy in its midst [and] spread out from its origin on Earth."

It's as well to mention at this point that, in 2005, Mikhail Gorbachev personally congratulated Kurzweil for foreseeing the pivotal role of communications technology in the collapse of the Soviet Union, and that Microsoft chairman Bill Gates calls him "the best person I know at predicting the future of artificial intelligence". A man of lesser accomplishments, touting the same head-spinning claims, would impress few beyond an inner circle of sci-fi obsessives, but Kurzweil – honoured as an inventor by US presidents Lyndon B Johnson and Bill Clinton – has rightfully earned himself a stockpile of credibility.

In person, chewing pensively on a banana, the softly spoken, slightly built Kurzweil looks chipper for his 61 years, and wears an elegantly tailored suit. A father of two, he resides in the Boston suburbs with his psychologist wife, Sonya, but has flown into Los Angeles for a private screening of Transcendent Man, the upcoming documentary that examines his life and theories over a suitably cosmic score by Philip Glass. "People don't really get their intellectual arms around the changes that are happening," he says, perched lightly on the edge of a large armchair, his overall sheen of wellbeing perhaps a shade more encouraging than you'd expect from a man of his age. "The issue is not just [that] something amazing is going to happen in 2045," he says. "There's something remarkable going on right now."

To understand exactly what he means, and why he thinks that his predictions bear up to hard scrutiny, it's necessary to return to the title of the above-mentioned book, and the grand idea on which it's based: "the singularity".

Borrowed from black-hole physics, in which the singularity is taken to signify what is unknowable, the term has been applied to technology to suggest that we haven't really got a clue what's going to happen once machines are vastly more "intelligent" than humans. The singularity, writes Kurzweil, is "a future period during which the pace of technological change will be so rapid, its impact so deep, that human life will be irreversibly transformed". He is not unique in his adoption of the idea – the information theorist John von Neumann hinted at it in the 1950s; retired maths professor and sci-fi author Vernor Vinge has been exploring it at length since the early 1980s – but Kurzweil's version is currently the most popular "singularitarian" text.

"I didn't come to these ideas because I had certain conclusions and worked backwards," he explains. "In fact, I didn't start looking for them at all. I was looking for a way to time my inventions and technology projects as I realised timing was the critical factor to success. And I made this discovery that if you measure certain underlying properties of information technology, it follows exquisitely predictable trajectories."

For Kurzweil, the crux of the singularity is that the pace of technology is increasing at a super-fast, exponential rate. What's more, there's also "exponential growth in the rate ' of exponential growth". It is this understanding that gives him the confidence to believe that technology – through an explosion of progress in genetics, nanotechnology and robotics – will soon surpass the limits of his imagination.

It is also why, in addition to bananas and the odd beneficial glass of red wine, he follows a regime of around 200 vitamin pills daily: not so much a diet as an attempt to "aggressively re-programme" his biochemistry. He claims that tests have shown he aged only two biological years over the course of 16 actual vitamin-popping years. He also says that, thanks to the regime, he has effectively cured himself of Type 2 diabetes. Not even open-heart surgery, which he underwent last year, and from which he made a rapid recovery ("a few hours later I was in the next room, and sent an email") could dent his convictions. On the contrary, he thinks that the brevity of his convalescence is proof positive that the pills are working. If he slows down the ageing process, he reckons, he'll be around long enough to witness the arrival of technology that will prolong his life... forever.

Kurzweil was raised in Queens, New York, where two youthful obsessions – electronics and music – would lead to a guest appearance on the 1960s TV quiz show I've Got a Secret, on which (aged 17) he showcased his first major invention: a home-made computer that could compose tunes. Five years later came the death (in 1970, when Ray was 22) of his father, Fredric, a struggling composer and conductor who, Kurzweil believes, never really got his due. "I'm painfully aware of the limitations he had, which were not his fault," he says. "In that generation, information about health was not very available, and we didn't have [today's] resources for creating music. Now, a kid in a dorm room can create a whole orchestral composition on a synthesizer."

The tragedy of that loss – and the fact that the means to repair a congenital heart defect were available to him, but not his father – is clearly an intense motivation for Kurzweil. Sometime soon, he believes, he will once again be able to converse with his father, such is the potential of the scientific advances he believes will ultimately pave the way to the singularity. Not everyone, though, concurs with his appraisal of technological progress, and his belief in the imminence of immortality.

Memorably, in the Transcendent Man documentary, Kevin Kelly, founding editor of future-thinking magazine Wired, labels Kurzweil a "deluded dreamer" who is "performing the services of a prophet". In reacting to that assessment, Kurzweil's habitually mellow tone of voice takes on a hint – albeit mild – of umbrage. "It's interesting that [Kelly] says my views are 'hard-wired', when I actually think his views are hard-wired," he says. "He's a linear thinker, and linear thinking is hard-wired in our brains: it worked very well 1,000 years ago. Some people really are resistant to accepting this exponential perspective, and they're very smart people. You show them the data, and yes, they follow it, but they just cannot get past it. Other people accept it readily."

Whereas Kelly differs from Kurzweil on the grounds of interpretation and tone, other voices of dispute are rooted in a deep-seated fear of technological calamity. "The form of opposition from fundamentalist humanists, and fundamentalist naturalists – that we should make no change to nature [or] to human beings – is directly contrary to the nature of human beings, because we are the species that goes beyond our limitations," counters Kurzweil. "And I think that's quite a destructive school of thought – you can show that hundreds of thousands of kids went blind in Africa due to the opposition to [genetically engineered] golden rice. The opposition to genetically modified organisms is just a blanket, reflexive opposition to the idea of changing nature. Nature, and the natural human condition, generates tremendous suffering. We have the means to overcome that, and we should deploy it."

To those opponents who detect a thick strain of techno-evangelism in Kurzweil's basically optimistic interpretation of the singularity, he reacts with self-parody: there's a tongue-in-cheek photo in The Singularity is Near of the author wearing a sandwich board bearing the book's title, and he insists he was never "searching for an alternative to customary faith". At the same time, he says humankind's inevitable move towards non-biological intelligence is "an essentially spiritual undertaking".

Whether or not he attracts a significant following of dedicated believers in search of deliverance, ecstasy or any variation thereof (some commentators have called the singularity "the rapture for geeks"), Kurzweil has undoubtedly positioned himself at the heart of a growing singularity industry. He is a director of the non-profit Singularity Institute for Artificial Intelligence, "the only organisation that exists for the expressed purpose of achieving the potential of smarter-than-human intelligence safer and sooner"; there's a second film awaiting release (part fiction, part documentary, co-produced by Kurzweil), also based on The Singularity is Near; and in addition to his theoretical books, he has co-authored a series of health titles, including Transcend: Nine Steps to Living Well Forever and Fantastic Voyage: Live Long Enough to Live Forever. The secret of immortality, he wants you to know, is available in book form.

Those who have lent Kurzweil their support include space-travel pioneer Peter Diamandis, chairman of the X-Prize Foundation; videogame designer (and creator of Spore and SimCity) Will Wright; and Nobel Prize-winning astrophysicist George Smoot. All three can be found on the faculty and adviser list of the recently founded Singularity University (Silicon Valley), of which Kurzweil is chancellor and trustee.

If the pace of technology continues to accelerate, as Kurzweil predicts, it seems likely that discussion of the singularity will see an exponential growth of its own. Few would dispute that it's one of the 21st century's most compelling ideas, because it connects issues that intensely polarise people (God, the energy crisis, genetic engineering) with sci-fi concepts that stir the imagination (artificial intelligence, immersive virtual reality, molecular engineering). Thanks largely to Kurzweil and the singularity, scenarios once viewed as diverting entertainment are being reappraised with a new seriousness. The line between fanciful thinker and credible, scientific analyst is becoming blurred: what once would have been relegated to the realms of sci-fi is now gaining factual currency.

"People can wax philosophically," says Kurzweil. "It's very abstract – whether it's a good thing to overcome death or not – but when it comes to some new methodology that's a better treatment for cancer, there's no controversy. Nobody's picketing doctors who put computers inside people's brains for Parkinson's: it's not considered controversial."

Might that change as more people become aware of the singularity and the pace of technological change? "People can argue about it," says Kurzweil, relaxed as ever within his aura of certainty. "But when it comes down to accepting each step along the way, it's done really without much debate."

'Transcendent Man' (transcendentman.com) screens at Sheffield Doc/Fest (0114 276 5141, sheffdocfest.com), running in association with 'The Independent', from 4-8 November

The greatest thing since sliced bread?

Ray Kurzweil's guide to incredible future technologies — and when he thinks they're likely to arrive...

1 Reconnaissance dust

"These so-called 'smart dust' – tiny devices that are almost invisible but contain sensors, computers and communication capabilities – are already being experimented with. Practical use of these devices is likely within 10 to 15 years"

2 Nano assemblers

"Basically, these are three-dimensional printers that can create a physical object from an information file and inexpensive input materials. So we could email a blouse or a toaster or even the toast. There is already an industry of three-dimensional printers, and the resolution of the devices that can be created is getting finer and finer. The nano assembler would assemble devices from molecules and molecular fragments, and is about 20 years away"

3 Respirocytes

"A respirocyte is a nanobot (a blood cell-sized device) that is designed to replace our biological red blood cells but is 1,000 times more capable. If you replaced a portion of your biological red blood cells with these robotic versions you could do an Olympic sprint for 15 minutes without taking a breath, or sit at the bottom of a swimming pool for four hours. These are about 20 years away" '

4 Foglets

"Foglets are a form of nanobots that can reassemble themselves into a wide variety of objects in the real world, essentially bringing the rapid morphing qualities of virtual reality to real reality. Nanobots that can perform useful therapeutic functions in our bodies, essentially keeping us healthy from inside, are only about 20 years away. Foglets are more advanced and are probably 30 to 40 years away"

5 Blue goo

"The concern with full-scale nanotechnology and nanobots is that if they had the capability to replicate in a natural environment (as bacteria and other pathogens do), they could destroy humanity or even all of the biomass. This is called the grey goo concern. When that becomes feasible we will need a nanotechnology immune system. The nanobots that would be protecting us from harmful self-replicating nanobots are called blue goo (blue as in police). This scenario is 20 to 30 years away"

Original article by Mike Hodgkinson for The Independent

Scientists Cure Color Blindness In Monkeys

2009-09-27T00:48:00.002-04:00

A test for color blindness showing a "6". Scientists used gene therapy to cure two squirrel monkeys of color blindness -- the most common genetic disorder in people. (Credit: iStockphoto/Thomas Pullicino)

Researchers from the University of Washington and the University of Florida used gene therapy to cure two squirrel monkeys of color blindness — the most common genetic disorder in people.

Writing online September 15 in the journal Nature, scientists cast a rosy light on the potential for gene therapy to treat adult vision disorders involving cone cells — the most important cells for vision in people.

"We've added red sensitivity to cone cells in animals that are born with a condition that is exactly like human color blindness," said William W. Hauswirth, Ph.D., a professor of ophthalmic molecular genetics at the UF College of Medicine and a member of the UF Genetics Institute and the Powell Gene Therapy Center. "Although color blindness is only moderately life-altering, we've shown we can cure a cone disease in a primate, and that it can be done very safely. That's extremely encouraging for the development of therapies for human cone diseases that really are blinding."

The finding is also likely to intrigue millions of people around the world who are colorblind, including about 3.5 million people in the United States, more than 13 million in India and more than 16 million in China. The problem mostly affects men, leaving about 8 percent of Caucasian men in the United States incapable of discerning red and green hues that are important for everyday things like recognizing traffic lights.

"People who are colorblind feel that they are missing out," said Jay Neitz, Ph.D., a professor of ophthalmology at the University of Washington. "If we could find a way to do this with complete safety in human eyes, as we did with monkeys, I think there would be a lot of people who would want it. Beyond that, we hope this technology will be useful in correcting lots of different vision disorders."

The discovery comes about 10 years after Neitz and his wife Maureen Neitz, Ph.D., a professor of ophthalmology at the University of Washington and senior author of the study, began training two squirrel monkeys named Dalton and Sam.

In addition to teaching the animals, the Neitz research group worked with the makers of a standard vision-testing technique called the Cambridge Colour Test to perfect a way the monkeys could "tell" them which colors they were seeing.

The tests are similar to ones given to elementary children the world over, in which students are asked to identify a specific pattern of colored dots among a field of dots that vary in size, color and intensity. The researchers devised a computer touch screen the monkeys could use to trace the color patterns. When the animals chose correctly, they received a reward of grape juice.

Likewise, decades were spent by Hauswirth and colleagues at the University of Florida to develop the gene-transfer technique that uses a harmless adeno-associated virus to deliver corrective genes to produce a desired protein.

In this case, researchers wanted to produce a substance called long-wavelength opsin in the retinas of the monkeys. This particular form of opsin is a colorless protein that works in the retina to make pigments that are sensitive to red and green.

"We used human DNAs, so we won't have to switch to human genes as we move toward clinical treatments," said Hauswirth, who is also involved in a clinical trial with human patients to test gene therapy for the treatment of Leber congenital amaurosis, a form of blindness that strikes children.

About five weeks after the treatment, the monkeys began to acquire color vision, almost as if it occurred overnight.

"Nothing happened for the first 20 weeks," Neitz said. "But we knew right away when it began to work. It was if they woke up and saw these new colors. The treated animals unquestionably responded to colors that had been invisible to them."

It took more than a year and a half to test the monkeys' ability to discern 16 hues, with some of the hues varying as much as 11-fold in intensity.

Dalton is named for John Dalton, an English chemist who realized he was colorblind and published the first paper about the condition in 1798.

"We've had Dalton and Sam for 10 years. They are like our children," Neitz said. "This species are friendly, docile monkeys that we just love. We think it is useful to continue to follow them — it's been two years now that they've been seeing in color, and continuing to check their vision and allowing them to play with the computer is part of their enrichment."

With the discovery, the researchers are the first to address a vision disorder in primates in which all photoreceptors are intact and healthy, providing a hint of gene therapy's full potential to restore vision.

About 1 in 30,000 Americans have a hereditary form of blindness called achromatopsia, which causes nearly complete color blindness and extremely poor central vision. "Those patients would be targets for almost exactly the same treatment," Hauswirth said.

Even in common types of blindness such as age-related macular degeneration and diabetic retinopathy, vision could potentially be rescued by targeting cone cells, he said.

"The major thrust of the study is you can ameliorate if not cure color blindness with gene therapy," said Gerald H. Jacobs, Ph.D., a research professor of psychology at the University of California, Santa Barbara, who was not involved in the research. "There are still questions about safety, but in these monkeys at least, there were no untoward effects. Those who are motivated to ameliorate their color defect might take some hope from the findings.

"This is also another example of how utterly plastic the visual system is to change," Jacobs said. "The nervous system can extract information from alterations to photopigments and make use of it almost instantaneously."

Adapted from materials provided by University of Florida.

Brain Health Tip #9

2009-09-25T08:20:00.002-04:00

Honing Your Brain For Irrelevance?

Bombarding yourself with media may affect your brain negatively and in ways you might not imagine. A study has shown that those who regularly switch from one tech task to another, such as constantly toggling windows to gaze at Facebook pages or IMing friends, are so tuned into irrelevancy that they are unable to concentrate when required.

According to a study done at Stanford, when students attended to technological stimuli throughout the day, it made it nearly impossible to tune those distractors out when an sustained attention dependent task was presented.

Students who were less inclined towards habitual multitasking were better able to organize memories, ignore elements of tests when required, and redirect focus quickly. As an antidote to a social landscape that might require more multitasking than not, students should practice sustained attention activities!

Brain Tip Courtesy of Luminosity.com

A Turning Point for Personal Genomes

2009-09-24T12:44:00.002-04:00

Scientists are finally starting to find medical information of value.

Last year, when more than 100 of the world's top geneticists, technologists, and clinicians converged on Cold Spring Harbor Laboratory in New York for the first annual Personal-Genomes conference, the main focus was James Watson's genome. The codiscoverer of the structure of DNA was the first to have his genome sequenced and published (aside from Craig Venter, who used his own DNA for the private arm of the human genome project.) Watson sat in the front row of the lecture hall as scientists presented their analysis of his genome. They paid special attention to the number of single-letter variations or small insertions and deletions in his DNA--clues as to whether he had a genetic variation that slightly boosted his risk for heart disease or cancer. But there was very little usable information in the genome.

Credit: Technology Review

That has all changed. In the last year, the number of sequenced, published genomes has shot up from two or three to approximately nine, with another 40 or so genomes sequenced but not yet published. "While the numbers are still small numbers, we are starting to put this research into the real disease context and get something out of it," says Jay Shendure, a geneticist at the University of Washington in Seattle, and a TR35 winner in 2006.

Last year, sequencing a genome was still a feat in itself, and much of the conference focused on the technical details--assessing accuracy and error rates and comparing one method to another. While these issues are still of central importance, sequencing a human genome has become routine enough to generate medically useful information. "Now we are able to do things automatically, so the biology starts to come out," says Paul Flicek, a bioinformaticist with the European Bioinformatics Institute and one of the conference organizers.

In a few cases, scientists have already been able to find the genetic cause of a disorder by sequencing an affected person's genome. Shendure has sequenced the coding region--the 1 percent of the genome that directs production of proteins--of the genomes of a handful of families with children afflicted with a rare inherited disorder called Miller Syndrome, which is linked to facial and limb abnormalities. Researchers compiled a list of genetic variations in each person and filtered out those that have been commonly found in people without the disease variations. They then looked for variants present only in affected people, and came up with one candidate gene. Shendure declined to identify the gene prior to publishing the findings, but noted that it was one they would not have anticipated. He hopes the technique can be applied to more common diseases as well, perhaps by studying people with early onset or extreme cases.

Original article written By Emily Singer for MIT Technology Review

Junk DNA may prove invaluable in quest for gene therapies

2009-09-23T11:56:00.001-04:00

Scientists have identified how a protein enables sections of so-called junk DNA to be cut and pasted within genetic code - a finding which could speed development of gene therapies.

The study by researchers at the University of Edinburgh sheds light on the process, known as DNA transposition, in which shifted genes have a significant effect on the behaviour of neighbouring genes. In the human genome, rearrangement of antibody genes can enable the immune system to target infection more effectively.

The research identifies how the enzyme is able to cut out a section of DNA and reinsert it elsewhere in the genome. The study, published in the journal Cell, was funded by the Wellcome Trust and the Medical Research Council.

The cut-and-paste property of shifted DNA is now being used to develop tools for scientific research and medical applications. Learning more about transposition could help scientists understand how to control the process and speed the development of gene therapies - which introduce into cells genes with beneficial properties that, for example, can fight hereditary diseases or cancer.

Junk DNA, which accounts for almost half of the human genome, was originally believed to have no purpose. However, it is now emerging that movement of junk DNA, in a cut-and-paste mechanism, can lead to beneficial changes in cells.

Dr Julia Richardson of the University's School of Biological Sciences, who led the study, said: "By forming a picture of the enzyme that causes DNA to shift, and discovering how this works, we understand more about how these proteins could be adapted and controlled. This may one day enable genes to be pasted into cells exactly where they are needed - which could be of enormous benefit in developing gene therapies."

Source: University of Edinburgh

Scientists Make Paralyzed Rats Walk Again After Spinal-cord Injury

2009-09-21T14:57:00.003-04:00

A combination of drugs, electrical stimulation and regular exercise can enable paralyzed rats to walk and even run again, researchers have discovered. (Credit: iStockphoto/Dmitry Maslov)

UCLA researchers have discovered that a combination of drugs, electrical stimulation and regular exercise can enable paralyzed rats to walk and even run again while supporting their full weight on a treadmill.

Published Nov. 20 in the online edition of Nature Neuroscience, the findings suggest that the regeneration of severed nerve fibers is not required for paraplegic rats to learn to walk again. The finding may hold implications for human rehabilitation after spinal cord injuries.

"The spinal cord contains nerve circuits that can generate rhythmic activity without input from the brain to drive the hind leg muscles in a way that resembles walking called 'stepping,'" explained principal investigator Reggie Edgerton, a professor of neurobiology and physiological sciences at the David Geffen School of Medicine at UCLA.

"Previous studies have tried to tap into this circuitry to help victims of spinal cord injury," he added. "While other researchers have elicited similar leg movements in people with complete spinal injuries, they have not achieved full weight-bearing and sustained stepping as we have in our study."

Edgerton's team tested rats with complete spinal injuries that left no voluntary movement in their hind legs. After setting the paralyzed rats on a moving treadmill belt, the scientists administered drugs that act on the neurotransmitter serotonin and applied low levels of electrical currents to the spinal cord below the point of injury.

The combination of stimulation and sensation derived from the rats' limbs moving on a treadmill belt triggered the spinal rhythm-generating circuitry and prompted walking motion in the rats' paralyzed hind legs.

Daily treadmill training over several weeks eventually enabled the rats to regain full weight-bearing walking, including backwards, sideways and at running speed. However, the injury still interrupted the brain's connection to the spinal cord-based rhythmic walking circuitry, leaving the rats unable to walk of their own accord.

Neuro-prosthetic devices may bridge human spinal cord injuries to some extent, however, so activating the spinal cord rhythmic circuitry as the UCLA team did may help in rehabilitation after spinal cord injuries.

The study was funded by the Christopher and Dana Reeve Foundation, Craig Nielsen Foundation, National Institute of Neurological Disorders and Stroke, U.S. Civilian Research and Development Foundation, International Paraplegic Foundation, Swiss National Science Foundation and the Russian Foundation for Basic Research Grants.
Adapted from materials provided by University of California - Los Angeles, via EurekAlert!, a service of AAAS.

Original article published in Science Daily

Direct Evidence Of Role Of Sleep In Memory Formation Is Uncovered

2009-09-17T19:10:00.003-04:00

For the first time, researchers have pinpointed the mechanism that takes place during sleep that causes learning and memory formation to occur. (Credit: iStockphoto/Mads Abildgaard)

ScienceDaily (Sep. 16, 2009) — A Rutgers University, Newark and Collége de France, Paris research team has pinpointed for the first time the mechanism that takes place during sleep that causes learning and memory formation to occur.

It’s been known for more than a century that sleep somehow is important for learning and memory. Sigmund Freud further suspected that what we learned during the day was “rehearsed” by the brain during dreaming, allowing memories to form. And while much recent research has focused on the correlative links between the hippocampus and memory consolidation, what had not been identified was the specific processes that cause long-term memories to form.

As posted online September 11, 2009 by Nature Neuroscience, György Buzsaki, professor at the Center for Molecular and Behavioral Neuroscience at Rutgers University, Newark, and his co-researchers, Gabrielle Girardeau, Karim Benchenane, Sidney I. Wiener and Michaël B. Zugaro of the Collége de France, have determined that short transient brain events, called “sharp wave ripples,” are responsible for consolidating memory and transferring the learned information from the hippocampus to the neocortex, where long-term memories are stored.

Sharp wave ripples are intense, compressed oscillations that occur in the hippocampus when the hippocampus is working “off-line,” most often during stage four sleep, which, along with stage three, is the deepest level of sleep.

During stage four sleep, Buzsaki explains, “it’s as if many instruments and members of the orchestra come together to generate a loud sound, a sound so loud that it is heard by wide areas of the neocortex. These sharp, ‘loud’ transient events occur hundreds to thousands of times during sleep and ‘teach’ the neocortex to form a long-term form of the memory, a process referred to as memory consolidation.” The intensity and multiple occurrence of those ripples also explain why certain events may only take place once in the waking state and yet can be remembered for a lifetime, adds Buzsaki.

The researchers were able to pinpoint that sharp wave ripples are the cause behind memory formation by eliminating those ripple events in rats during sleep. The rats were trained in a spatial navigation task and then allowed to sleep after each session. Those rats that selectively had all ripple events eliminated by electrical stimulation were impeded in their ability to learn from the training, as compressed information was unable to leave the hippocampus and transfer to the neocortex.

Identification of a specific brain pattern responsible for strengthening learned information could facilitate applied research for more effective treatment of memory disorders.

“This is the first example that if a well-defined pattern of activity in the brain is reliably and selectively eliminated, it results in memory deficit; a demonstration that this specific brain pattern is the cause behind long-term memory formation,” says Buzsaki.

The research also represents a move toward a new direction in neuroscience research. While previous research largely has focused on correlating behavior with specific brain events through electroencephalogram, neuronal spiking and functional magnetic resonance imaging studies, increasingly researchers are challenging those correlations as they seek to identify the specific process or processes that cause certain events and behaviors to take place.

The research was performed at the Collége de France, Paris where Buzsaki worked as a distinguished visiting professor in 2008.

Journal reference:

Gabrielle Girardeau, Karim Benchenane, Sidney I Wiener, György Buzsáki & Michaël B Zugaro. Selective suppression of hippocampal ripples impairs spatial memory. Nature Neuroscience, 2009; DOI: 10.1038/nn.2384

Adapted from materials provided by Rutgers University.

Originally Posted in Science Daily

Research like this progresses further the possibility that in the near future uploading or copying the brain's memories and thus the individual (consciousness) into another body.

MORE EVIDENCE FOR ANTIOXIDANTS

2009-09-16T13:15:00.003-04:00

In a study that will provide comfort to chocoholics everywhere, researchers in Sweden have found evidence that people who eat chocolate have increased survival rates after a heart attack — and it may be that the more they eat, the better.

Andrew Rodriguez

Chocolate consumption and mortality following a first acute myocardial infarction: the Stockholm Heart Epidemiology Program (Journal of Internal Medicine)

The scientists followed 1,169 nondiabetic men and women who had been hospitalized for a first heart attack. Each filled out a standardized health questionnaire that included a question about chocolate consumption over the past 12 months. Chocolate contains flavonoid antioxidants that are widely believed to have beneficial cardiovascular effects.

The patients had a health examination three months after their discharge from the hospital, and researchers followed them for the next eight years using Swedish national registries of hospitalizations and deaths. After controlling for age, sex, obesity, physical inactivity, smoking, education and other factors, they found that the more chocolate people consumed, the more likely they were to survive. The results are reported in the September issue of The Journal of Internal Medicine.

But before concluding that a box of Godiva truffles is health food, chocolate lovers may want to consider some of the study’s weaknesses. It is an observational study, not a randomized trial, so cause and effect cannot be definitively established.

Even though the researchers controlled for many variables, chocolate consumption could be associated with factors they did not account for — mental health, for example — that might reduce the risk for death.

The scientists did not ask what kind of chocolate the patients ate, and milk chocolate has less available flavonoid than dark chocolate. Finally, chocolate consumption did not reduce the risk for any nonfatal cardiac event.

Still, Dr. David L. Katz, an associate professor of public health at Yale who was not involved in the work, said the study added “an interesting element, following a group of adults who’ve had a heart attack and noting an impressive reduction in cardiac deaths.” While the study is observational, he said, “the broader context is reassuring.”

While the chocolate eaters in the study had a statistically insignificant reduction in the risk of death from any cause over the eight-year span, the reduced risk for dying of heart disease was highly significant. And it was dose-dependent — that is, the more chocolate consumed, the lower the risk for death.

Compared with people who ate none, those who had chocolate less than once a month had a 27 percent reduction in their risk for cardiac death, those who ate it up to once a week had a 44 percent reduction and those who indulged twice or more a week had a 66 percent reduced risk of dying from a subsequent heart event. The beneficial effect remained after controlling for intake of other kinds of sweets.

A co-author of the paper, Dr. Kenneth J. Mukamal, an associate professor of medicine at Harvard, said that there was considerable data from other studies suggesting that chocolate lowered blood pressure and that this might be a cause of the lower cardiac mortality found in the study.

Dr. Katz, of Yale, agreed that “there are many reasonable biological mechanisms” for a protective effect from chocolate.

“I like the study,” he said. “It adds to the general fund of knowledge we already have.”

Dr. Mukamal sounded a note of caution about the findings.

“Although this is interesting and provocative, chocolate does not come without costs,” he said. “For people looking for a small snack to finish a meal, this is a great choice. But it should be supplementing healthy eating and replacing less healthy snacks.”

Originally posted in New york times

Master Gene That Switches On Disease-fighting Cells Identified By Scientists

2009-09-15T15:18:00.001-04:00

The master gene that causes blood stem cells to turn into disease-fighting 'Natural Killer' (NK) immune cells has been identified by scientists, in a study published in Nature Immunology Setember 13. The discovery could one day help scientists boost the body's production of these frontline tumour-killing cells, creating new ways to treat cancer.

The researchers have 'knocked out' the gene in question, known as E4bp4, in a mouse model, creating the world's first animal model entirely lacking NK cells, but with all other blood cells and immune cells intact. This breakthrough model should help solve the mystery of the role that Natural Killer cells play in autoimmune diseases, such as diabetes and multiple sclerosis. Some scientists think that these diseases are caused by malfunctioning NK cells that turn on the body and attack healthy cells, causing disease instead of fighting it. Clarifying NK cells' role could lead to new ways of treating these conditions.

The study was carried out by researchers at Imperial College London, UCL and the Medical Research Council's National Institute for Medical Research.

Natural Killer cells – a type of white blood cell - are a major component of the human body's innate, quick-response immune system. They provide a fast frontline defence against tumours, viruses and bacterial infections, by scanning the human body for cells that are cancerous or infected with a virus or a bacterial pathogen, and killing them.

NK cells - along with all other types of blood cell, both white and red - are continuously generated from blood stem cells in the bone marrow over the course of a person's lifetime. The gene E4bp4 identified in today's study is the 'master gene' for NK cell production, which means it is the primary driver that causes blood stem cells to differentiate into NK cells.

The researchers behind this new study, led by Dr Hugh Brady from the Department of Life Sciences at Imperial College London, are hoping to progress with a drug treatment for cancer patients which reacts with the protein expressed by their E4bp4 gene, causing their bodies to produce a higher number of NK cells than normal, to increase the chances of successfully destroying tumours.

Currently, NK cells isolated from donated blood are sometimes used to treat cancer patients, but the effectiveness of donated cells is limited because NK cells can be slightly different from person to person. Dr Brady explains: "If increased numbers of the patient's own blood stem cells could be coerced into differentiating into NK cells, via drug treatment, we would be able to bolster the body's cancer-fighting force, without having to deal with the problems of donor incompatibility."

Dr Brady and his colleagues at the MRC National Institute for Medical Research proved the pivotal role E4bp4 plays in NK production when they knocked the gene out in a mouse model. Without E4bp4 the mouse produced no NK cells whatsoever but other types of blood cell were unaffected. As well as proving their hypothesis about the function of the E4bp4 gene, this animal model will allow medical researchers, for the first time, to discover if NK cell malfunction is behind a wide range of medical conditions, including autoimmune disorders, inflammatory conditions, persistent viral infections, female infertility and graft rejection.

Dr Brady explains: "Since shortly after they were discovered in the 1970s some scientists have suspected that the vital disease-fighting NK cells could themselves be behind a number of serious medical conditions, when they malfunction. Now finally, with our discovery of the NK cell master gene and subsequent creation of our mouse model, we will be able to find out if the progression of these diseases is impeded or aided by the removal of NK cells from the equation. This will solve the often-debated question of whether NK cells are always the 'good guys', or if in certain circumstances they cause more harm than good."

The researchers were initially studying the effect of E4bp4 in a very rare but fatal form of childhood leukaemia when they discovered its importance for NK cells.

The study was funded by the charities CHILDREN with LEUKAEMIA and Leukaemia Research.

Posted in ScienceDaily (Sep. 14, 2009)

Lowering sodium consumption could save US $18 billion annually in health costs

2009-09-14T18:53:00.000-04:00

Reducing Americans' average intake of sodium to the amount recommended by health officials could save the nation as much as $18 billion annually in avoided health care costs and improve the quality of life for millions of people, according to a new RAND Corporation study.

The study estimates that meeting national sodium guidelines could eliminate 11 million cases of high blood pressure nationally and extend the lives of thousands of people each year. The monetary value of the improved quality of life would be an estimated $32 billion annually, according to the findings published in the September/October edition of the Journal of Health Promotion.

"This study provides an important first step toward quantifying the benefits of reducing the intake of sodium by the American public," said Kartika Palar, the study's lead author and a graduate fellow at the RAND Pardee Graduate School. "These findings make a strong case that there's value in pursuing a population-based approach to reducing sodium intake among Americans."

The study is one of the first to estimate the economic benefits of lowering sodium consumption among the American public.

Excessive consumption of sodium is a persistent health problem in the United States, causing increased rates of high blood pressure and related illnesses such as cardiovascular diseases. The Institute of Medicine recommends that adults consume no more than 2,300 milligrams of sodium each day, with lower amounts recommended for older adults, black patients and those with high blood pressure -- groups that are at higher risk.

Researchers from RAND Health analyzed information about Americans' blood pressure levels, use of antihypertensive medications and sodium intake from the National Health and Nutrition Examination Survey, a federal study that routinely assesses the health and nutritional status of adults and children in the United States. The study is unique in that it combines interviews and physical examinations.

Palar and study co-author Roland Sturm, a RAND senior economist, using a cross-sectional simulation model, calculated that lowering sodium intake would trim a sizable portion of the $55 billion spent nationally each year to treat high blood pressure. About half of the $18 billion in annual health care cost savings would accrue to public sector health spending. Researchers say their estimates are conservative because they were not able to calculate the savings for illnesses such as cardiovascular diseases where sodium consumption plays a less-defined role.

In addition, researchers estimated that meeting sodium consumption guidelines would save in one year 312,000 quality adjusted life years -- a research measurement that adjusts increased longevity for the relative healthiness experienced during additional years of life.

"Our results are driven by the fact that nearly 30 percent of the nation's population has hypertension," Palar said. "One of the reasons that hypertension is so pervasive is that sodium consumption is so high."

Researchers say that better strategies for lowering sodium intake broadly across the nation's population still need to be developed. Studies estimate that more than 75 percent of Americans dietary sodium intake comes from processed foods rather than from salt added during cooking at home or at the dining table. Restaurant food also is generally high in sodium.

Population-based strategies that have been discussed include redesigning food labeling information to better highlight sodium levels, having manufacturers voluntarily lower sodium levels and adopting regulations that would require food processors to lower sodium.

Source: RAND Corporation

September 11th, 2009 in Medicine & Health / Health

Scientist: Human brain could be replicated in 10 years

2009-09-13T06:20:00.002-04:00

TO THE RIGHT:Activity in the brain's neocortex is tightly controlled by inhibitory neurons shown here which prevent epilepsy (Blue Brain Project; Ecole Polytechnique Federale de Lausanne)

A model that replicates the functions of the human brain is feasible in 10 years according to neuroscientist Professor Henry Markram of the Brain Mind Institute in Switzerland. ‘I absolutely believe it is technically and biologically possible. The only uncertainty is financial. It is an extremely expensive project and not all is yet secured.'

The apparent complexity of the human mind is not a barrier to building a ‘replica' brain claims Professor Markram. ‘The brain is of course extremely complex because it has trillions of synapses, billions of neurons, millions of proteins, and thousands of genes. But they are still finite in number. Today's technology is already highly sophisticated and it allows us to reverse engineer the brain rapidly'. An example of the capability already in place is that today's robots can do screenings and mappings tens of thousands of times faster than human scientists and technicians.

Another hurdle on the path to a model human brain is that 100 years of neuroscience discovery has led to millions of fragments of data and knowledge that have never been brought together and exploited fully. ‘Actually no- one even knows what we already understand about the brain', says Professor Markram, ‘A model would serve to bring this all together and then allow anyone to test whatever theory you want about the brain. The biggest challenge is to understand how electrical-magnetic-chemical patterns in the brain convert into our perception of reality. We think we see with our eyes, but in fact most of what we ‘see' is generated as a projection by your brain. So what are we actually looking at when we look at something ‘outside' of us?'

For Professor Markram, the most exciting part of his research is putting together the hundreds of thousands of small pieces of data that his lab has collected over the past 15 years, and seeing what a microcircuit of the brain looks like. ‘When we first switched it on it already started to display some interesting emergent properties. But this is just the beginning because we know now that it is possible to build it. As we progress we are learning about design secrets of our brains which were unimaginable before. In fact the brain uses some simple rules to solve highly complex problems and extracting each of these rules one by one is very exciting. For example we have been surprised at finding simple design principles that allow billions of neurons to connect to each other. I think we will understand how the brain is designed and works before we have finished building it'.

The opportunities for this neuroscience research challenge are immense explains Professor Markram: ‘A brain model will sit on a massive supercomputer and serve as a kind of educational and diagnostic service to society. As the industrial revolution in science progresses we will generate more data than anyone can track or any computer can store, so models that can absorb it are simply unavoidable. It is also essential to build models when it comes to treating brain diseases affecting around two billion people. At present, there is no brain disease for which we really understand what has gone wrong in the processing, in the circuits, neurons or synapses. It is also important if we are to replace the need for the millions of animal experiments each year for brain research'.

Source: Plataforma SINC (news : web)
pOSTED IN pHYSORG.COM

Threescore and 17.9: Longevity Rises

2009-09-11T21:23:00.001-04:00

Death rates are at a record low and life expectancy is at a record high in the United States, according to the latest figures from the Centers for Disease Control and Prevention.

Preliminary data for 2007, released on Aug. 19, show that death rates have decreased to 760.3 per 100,000 from 776.5 in 2006, and a baby born in 2007 can expect to live 77.9 years, compared with 77.7 for one born in 2006.

Age-adjusted death rates decreased significantly for 8 of the 15 leading causes of death: heart disease, cancer, cerebrovascular disease, accidents, diabetes, influenza, high blood pressure and assaults.

The decreases in death rate held across all races and ethnicities, with black males showing the largest decrease — more than 4 percent. The drop occurred in all age groups except infants under 1 year old, where rates were unchanged.

Kenneth D. Kochanek, a co-author of the report and a statistician with the National Center for Health Statistics, said the findings were welcome.

“We want all leading causes of death to go down and life expectancy to go up,” Mr. Kochanek said. “That’s good news, but it doesn’t make the front page of the paper because it’s nothing spectacular.”

Caloric Restriction Slows Aging in Monkeys

2009-09-10T14:37:00.002-04:00

The diet delays or prevents diabetes, cancer, heart disease, and brain atrophy.

A 20-year study involving rhesus monkeys has provided the first strong evidence that caloric restriction slows the aging process in primates.

Senior citizen: Canto, 27, is on a calorie-restricted diet as part of a study examining the effects of diet on aging.
Credit: University of Wisconsin Madison / Jeff Miller

A diet that's nutritionally adequate but provides 30 percent fewer calories than normal has been shown to extend life span and delay the onset of age-related diseases in other animals, including flies, worms, and rodents. But because studies on primates take much longer, the benefits had not yet been demonstrated to extend to them. Now researchers at the National Primate Research Center at the University of Wisconsin-Madison report that in rhesus monkeys, caloric restriction begun in adulthood reduces risk of the most common age-related conditions--diabetes, cancer, heart disease, and brain atrophy--by a third.

"With these results, we have become convinced that aging retardation is happening," says Richard Weindruch, a professor of medicine at the University of Wisconsin-Madison, who began the study in 1989. The research involved 76 monkeys, half of them on the extreme diet. By now, the 33 surviving monkeys have reached old age. Thirty-seven percent of the monkeys on a normal diet have died of age-related diseases, compared with just 13 percent of the monkeys on the restricted diet. It's still unknown whether caloric restriction extends the animals' life span, but the results published today in the journal Science detail the benefits of the diet in preventing the most common such diseases.

The strongest evidence from the study concerns metabolic disorders. While five of the monkeys on a normal diet became diabetic and 11 were prediabetic (having blood glucose levels higher than normal), monkeys on the restricted diet were completely free of the disease. The incidence of both cardiovascular disease and tumors was reduced by 50 percent in the diet group. And magnetic resonance imaging showed that caloric restriction preserved gray-matter volume in the brain as the monkeys aged. In general, the dieting group appeared to be biologically younger: age-related diseases, if they developed, occurred later in life.

The work is significant because rhesus monkeys are more closely related to humans than other animals used so far in studies of caloric restriction. "Monkeys are so closely related to us; it's a much easier jump that this is likely to work in humans," says Ricki Colman, a lead researcher on the study. The Wisconsin researchers also took pains to make the study as applicable to humans as possible. "We treat each animal as an individual patient," Colman says. The animals receive physical exams every six months, along with full dental care and medical interventions as needed. "We treat the diabetes with insulin, and when we identify tumors we remove them," she explains.

Audio »

Calorie consumption: The rhesus monkey on the left, Canto, eats a calorie-restricted diet and is 27 years old. The monkey on the right, Owen, consumes a normal diet and is 29.
Credit: University of Wisconsin-Madison / Jeff Miller

Of course, as Colman points out, "it's not a realistic goal for humans to practice caloric restriction." The ultimate goal of the study, she says, is to better understand the underlying mechanisms of aging in order to learn how people can live healthier, longer lives: "It's something we use to understand the aging process better."

There is some evidence that caloric restriction has metabolic and cardiovascular benefits in humans, but data from monkeys are important because these studies are difficult to perform in people, especially over the long term. "Human data are still sketchy--it's difficult to get controlled experiments in humans," says Leonard Guarente, a professor of biology at MIT. Even in monkeys, he says, "these are very difficult and long-, long-term studies to do."

Two big questions remain, the researchers say. First, does caloric restriction extend life span in the primates? "Meaningful maximum-life-span data are probably 15 years away," says Weindruch. The monkeys in the Wisconsin study fall into two age groups; the average age of the oldest group is 29, which is very old considering that these animals, on average, live to about 25 in captivity. However, the longest a rhesus monkey has been known to live is 40 years. "If the last of the monkeys on caloric restriction die at the same time as the last control monkeys, it means there is only a delay of the onset of disease, but not an extension of life span," says Luigi Fontana, a research professor at the Washington University School of Medicine in St. Louis who is leading a study of the diet in people.

The other unresolved question is how caloric restriction actually works in the monkeys. Now that they have strong evidence of the diet's benefits, Weindruch says, his group will establish another group of animals to study the underlying mechanisms.

Oringially posted in MIT tech review by Katherine Bourzac

Secrets of the centenarians: Life begins at 100

2009-09-08T14:12:00.002-04:00

THIS year, the number of pensioners in the UK exceeded the number of minors for the first time in history. That's remarkable in its own right, but the real "population explosion" has been among the oldest of the old - the centenarians. In fact, this is the fastest-growing demographic in much of the developed world. In the UK, their numbers have increased by a factor of 60 since the early 20th century. And their ranks are set to swell even further, thanks to the ageing baby-boomer generation: by 2030 there will be about a million worldwide.

These trends raise social, ethical and economic dilemmas. Are medical advances artificially prolonging life with little regard for the quality of that life? Old age brings an increased risk of chronic disease, disability and dementia, and if growing numbers of elderly people become dependent on state or familial support, society faces skyrocketing costs and commitments. This is the dark cloud outside the silver lining of increasing longevity. Yet researchers who study the oldest old have made a surprising discovery that presents a less bleak vision of the future than many anticipate.

It is becoming clear that people who break through the 90-plus barrier represent a physical elite, markedly different from the elderly who typically die younger than them. Far from gaining a longer burden of disability, their extra years are often healthy ones. They have a remarkable ability to live through, delay or entirely escape a host of diseases that kill off most of their peers. Supercentenarians - people aged 110 or over - are even better examples of ageing gracefully. "As a demographic group, they basically didn't exist in the 1970s or 80s," says Craig Willcox of the Okinawa Centenarian Study in Japan. "They have some sort of genetic booster rocket and they seem to be functioning better for longer periods of time than centenarians." The average supercentenarian had freely gone about their daily life until the age of 105 or so, some five to 10 years longer even than centenarians, who are themselves the physical equivalent of people eight to 10 years their junior. This isn't just good news for the oldest old and for society in general; it also provides clues about how more of us might achieve a long and healthy old age.

One of the most comprehensive studies comes from Denmark. In 1998, Kaare Christensen at the University of Southern Denmark, in Odense, exploited the country's exemplary registries to contact every single one of the 3600 people born in 1905 who was still alive. Assessing their health over the subsequent decade, he found that the proportion of people who managed to remain independent throughout was constantly around one-third of the total: each individual risked becoming more infirm, but the unhealthiest ones passed away at earlier ages, leaving the strongest behind. In 2005, only 166 of the people in Christensen's sample were alive, but one-third of those were still entirely self-sufficient (Proceedings of the National Academy of Sciences, vol 105, p 13274). This is good news from both personal and societal perspectives, for it means that exceptional longevity does not necessarily lead to exceptional levels of disability.

Christensen's optimistic findings are echoed in studies all over the world. In the US, almost all of the 700-plus people recruited to the New England Centenarian Study (NECS) since it began in 1994 had lived independently until the age of 90, and 40 per cent of supercentenarians in the study could still look after themselves. In the UK, Carol Brayne at the University of Cambridge studied 958 people aged over 90 and found that only one-quarter of them were living in institutions or nursing homes. Likewise, research in China reveals that before their deaths, centenarians and nonagenarians spend fewer days ill and bedridden than younger elderly groups, though the end comes quickly when it finally comes.

Distinctive minds

Of course, people can live independently without being entirely healthy, and it is true that most centenarians suffer from some sort of ailment. These range from osteoarthritis - which is almost universal and often omitted from studies - to simple loneliness. Neurodegenerative diseases are common too, with around 70 to 85 per cent of centenarians suffering from some form of dementia. But dementia in this group follows a different pattern to the general population. It is more likely to be vascular dementia or rare neurodegenerative conditions such as Pick's disease or Lewy body disease.

Alzheimer's disease, the most common form of dementia, is relatively rare among centenarians yet, intriguingly, autopsies reveal that the brains of the oldest old, who had shown no outward sign of dementia, are sometimes riddled with the lesions associated with Alzheimer's disease. The basis of this resilience to Alzheimer's is largely unknown. The simple fact is that many people who become centenarians seem able to tolerate damage that would significantly harm less robust individuals, and although many suffer from dementia as death draws near, most remain mentally agile well into their nineties.

Not all of the oldest old survive by delaying illness or disability, though - many soldier through it. Jessica Evert of Ohio State University in Columbus examined the medical histories of over 400 centenarians (The Journals of Gerontology Series A, vol 58, p 232). She found that those who achieve extreme longevity tend to fall into three categories. About 40 per cent were "delayers", who avoided chronic diseases until after the age of 80. This "compression of morbidity", where chronic illness and disability are squeezed into ever-shorter periods at the end of life, is a recent trend among ageing populations. Another 40 per cent were "survivors", who suffered from chronic diseases before the age of 80 but lived longer to tell the tale. The final 20 per cent were "escapers", who hit their century with no sign of the most common chronic diseases, including heart disease, cancer, diabetes, hypertension and stroke. Intriguingly, one-third of male centenarians were in this category, compared with only 15 per cent of women (see "Two paths to 100").

So what are the secrets of a long and healthy life? Gerontologists point to four key factors: diet, exercise, "psycho-spiritual" and social, so anyone aiming for a century should not underestimate the power of lifestyle - despite the odd centenarian who proudly claims to have smoked 60 cigarettes a day for decades. Thomas Perls, who heads the NECS, believes that up to 70 per cent of longevity is due to non-genetic factors (New Scientist, 3 June 2006, p 35). Nevertheless, many people who live well into old age do tend to have another advantage: an inherited genetic pass.

Take a close relative of a centenarian and you can put good money on their chances of living a long life. Among Americans born in 1900, brothers of centenarians were 17 times as likely to reach a century as their peers, and sisters, eight times. The New England study reveals that the children of centenarians are less than one-third as likely to die of cancer as the general population, and less than one-sixth as likely to die of heart disease.

Further evidence of a genetic link comes from longevity hotspots. Okinawa in Japan is the front runner. At 58 centenarians per 100,000 people (and rising), it has the world's highest proportion in this age group - more than five times the level of some developed countries. Like other hotspots, including Sardinia and Iceland, Okinawa is a relatively isolated island community, which leads to higher levels of inbreeding and a clustering of genetic variants. While such genetic similarity usually has detrimental effects, in these hotspots it seems to have united and maintained genetic variants that predispose people to a long life.

Of course, members of isolated communities or families usually share a particular environment too, but this alone cannot explain clusters of longevity. Gerontologists have found that the influence of environmental factors such as wealth or education on lifespan fades as we age, while that of genes increases. By comparing 10,000 pairs of Scandinavian twins, Christensen found that genes only start exerting a strong influence on our lifespan after the age of 60. Before then, both identical and non-identical twins have largely independent odds of reaching a given age. Beyond 60, however, the odds of one twin reaching a given age are greatly increased if their co-twin has done so, especially if the twins are identical (Human Genetics, vol 119, p 1432).

This makes the "centenarian genome" a key resource for identifying "longevity genes", an invaluable step in understanding the physiological processes underlying long lives. Such genes have been found in abundance in other organisms - including over 70 in the worm Caenorhabditis elegans. Unfortunately, it's a different story in humans. While many candidate genes have been suggested to affect lifespan, very few have been consistently verified in multiple populations.

The centenarian genome is a key resource in identifying longevity genes

Until recently, the only exception was ApoE, and in particular a variant of this gene known as e4, which bestows carriers with a much higher than average risk of developing Alzheimer's and heart disease. Across the world, this unfortunate version of ApoE is about half as common in centenarians as in younger adults. Last year, a second promising candidate emerged - a variant of a gene called FOXO3A. At the University of Hawaii, a team led by Bradley Willcox, Craig's identical twin, found that people who carried two copies of a particular form of the gene were almost three times as likely to make it to 100 than those without the variation, and also tended to start their journey into old age with better health and lower levels of stroke, heart disease and cancer (Proceedings of the National Academy of Sciences, vol 105, p 37). "There are so many false positives in this field that FOXO3A is very exciting," says Bradley Willcox.

FOXO3A is involved in several signalling pathways that are conserved across animal species. It controls the insulin/IGF-1 pathway, which influences how our bodies process food. It also controls genes that protect cells from highly reactive oxygen radicals - molecules often thought to drive human ageing through the cumulative damage they wreak on DNA. FOXO3A could even protect against cancer by encouraging apoptosis, whereby compromised cells commit suicide. The variant of FOXO3A associated with longevity is much more prevalent in 100-year-olds even than in 95-year-olds, which clearly demonstrates the value of studying the centenarian genome.

So far the search for longevity genes in humans has been extremely difficult, but prospects brighten as genomic technologies become faster and there are more centenarians to study. Only a lucky few win the genetic lottery of longevity, but if we understand what sets them apart, we may be able to make the rest of us more like them by using lifestyle or therapeutic interventions to manipulate physiological pathways. Such medical advances will not only extend our lives, but also help us remain healthy and independent for as long as possible.

Gallery: Six famous centenarians

Two paths to 100

The two sexes fare very differently in the longevity stakes. There are far more female centenarians than male ones, but men who do make it past 100 tend to be more physically robust and mentally sharper.

The reasons behind this are unclear. It may be simply that the female body is better able to tolerate chronic illnesses and disabilities as it ages. However, natural advantage cannot be the whole story as female centenarians are more likely than their male peers to have ridden to 100 on the back of healthy lifestyles.

"For all the major health hazards, women take better care of themselves," says Craig Willcox of Okinawa International University in Japan, who works on the Okinawa Centenarian Study. "They smoke less, drink less alcohol and are less likely to die of violent causes, accidents and suicides. They also go to their physician more."

Men, meanwhile, have the double disadvantage of being both more prone to risky behaviours throughout their lives and more likely to succumb to chronic illnesses as they age. This means that men who do make it to their century must depend more on genetic trump cards to see them through.

Dying of old age

"There is one, and only one, cause of death at older ages. And that is old age." So said Leonard Hayflick, one of the most influential gerontologists of all time. But dying of old age isn't just a case of peacefully losing the will to live - it is an accumulation of diseases and injuries different to those that tend to kill people at younger ages.

For a start, the oldest old have very low rates of chronic diseases such as cancer, heart disease and stroke. The trend is particularly apparent for cancer. The odds of developing it increase sharply as people age, but they fall from the age of 84, and plummet from 90 onwards. Only 4 per cent of centenarians die of cancer, compared with 40 per cent of people that die in their fifties and sixties.

Many centenarians even manage to ward off chronic diseases after indulging in a lifetime of serious health risks. Many people in the New England Centenarian Study experienced a century free of cancer or heart disease despite smoking as many as 60 cigarettes a day for 50 years. The same story applies to people from Japan's longevity hotspot, Okinawa, where around half of the local supercentenarians had a history of smoking and one-third were regular alcohol drinkers. These people may well have genes that protect them from the dangers of carcinogens or the random mutations that crop up naturally when cells divide.

So what does kill off the oldest old? Pneumonia is the biggest culprit, with other respiratory infections, accidents and intestinal problems trailing behind. "Dying of old age involves total systems failure," says Craig Willcox of the Okinawa Centenarian Study in Japan. "Centenarians avoid age-associated diseases, but you see a lot of systemic wear and tear. Almost all of them have had some problems with cataracts, they can't hear very well and have osteoarthritis. Our most recently deceased centenarian in Okinawa caught a cold and died in her sleep."

Ed Yong is a science writer based in London

This article was originally posted in new scientist

Gallery: Six famous centenarians

Breakthrough in 3-D Brain Mapping Enables Removal of Fist-Sized Tumor

2009-09-07T03:47:00.001-04:00

The surgery was performed at University Hospital by an eight-member team from the Brain Tumor Center at the UC Neuroscience Institute.

"This marks the culmination of one of the most important developments in brain tumor surgery in the last 100 years," says John Tew, MD, a neurosurgeon with the Mayfield Clinic, UC professor of neurosurgery and clinical director of the UC Neuroscience Institute.

The multiple brain scans were fused and installed into a surgical guidance computer, whose function is similar to a global positioning system. By revealing the tumor's relationship to all of the functional centers, electrical pathways and arteries and veins in the patient's brain, the technology enabled Tew and his team to map out a safe pathway to the tumor.

The processing and fusion of images was performed by James Leach, MD, associate professor of neuroradiology at UC, and a neuroradiologist at Cincinnati Children's Hospital Medical Center and the UC Neuroscience Institute, using the BrainLAB iPlan system at University Hospital.

"This fusion of images is exciting in that it allows us to maximize resection (removal) of the tumor while preserving function for the patient," Leach says.

Since early 2007 Brain Tumor Center specialists have used the fusion of three types of imaging as a guide to stereotactic surgery:

Magnetic resonance imaging (MRI), which creates detailed pictures of the body by detecting differences in magnetic signals between different types of tissues.
Functional magnetic resonance imaging (fMRI), which creates a series of images that capture blood oxygen levels in parts of the brain that are responsible for movement, perception and cognition.
Diffusion tensor imaging (DTI), which provides a map of critical white-matter tracts, which facilitate electrical connections between different parts of the brain.

In the latest development, Leach added the fusion of computed tomography angiography (CTA), which provides a map of blood vessels (arteries and veins).

"The ability to completely map the brain and to understand—before we operate—where the tumor lies in relation to important structures is a milestone in our use of digital computer technology to heighten patient safety during complex brain tumor surgery," Tew says.

The fMRI and DTI studies were performed on University Hospital's 3T MRI system. "The 3T system allows us to image the functional areas of the brain using various language, motor and vision tasks with the patient in the MRI scanner," Leach explains. "The addition of the DTI sequence allows the connections between these areas and other parts of the nervous system to be identified at the same time."

FMRI scanning takes approximately 75 minutes, about 30 minutes longer than traditional MRI. The DTI scan, which takes five minutes, is performed in the same setting.

CTA scanning was performed at University Hospital.

Leach processed the images, highlighting the location of speech and movement areas, white matter tracts and arteries and veins. He also highlighted the tumor location, then imported all of the information into BrainLAB's navigation software at University Hospital.

Assisted by the three-dimensional brain-mapping, Tew and his team were able to navigate a trajectory through the patient's brain and remove 90 percent of the malignant tumor, an anaplastic astrocytoma, without harming the healthy brain tissue—including the deep nerve-fiber tracts—that surrounded it. The patient was talking normally right after surgery, and she was walking the halls and able to take a shower without assistance one day after surgery.

The team sought to eradicate the remaining tumor by applying a course of 33 computer-guided, fractionated radiotherapy treatments as a first approach. During fractionated radiotherapy, a small burst of radiation is delivered to the lesion every day over a period of weeks. Delivering radiation in this way, rather than in a single, concentrated session, allows healthy tissue to recover in between treatment sessions. The patient underwent those treatments at the Precision Radiotherapy Center in West Chester.

Concurrently, the patient underwent treatment with a chemotherapy agent (temosolomide). If the radiotherapy and chemotherapy are not effective, she could face another operation.

Source: University of Cincinnati Academic Health Center
originally posted in physorg.com

Your Cyborg Eye Will Talk to You

2009-09-06T02:24:00.003-04:00

Just as many of us are getting used to augmented reality applications for cellphones and digital cameras, Babak Amir Parviz and his University of Washington students are taking it one step further. The group is working on a human machine interface where LEDs are embedded into contact lenses in order to display information to the wearer. You heard right, in a few years your cyborg eye will talk to you. In an article with the IEEE Spectrum, Parviz relays the challenges of custom-building semi-transparent circuitry into a polymer lens roughly 1.2 millimeters in diameter.

More News From ReadWriteWebSays Parviz, "We're starting with a simple product, a contact lens with a single light source, and we aim to work up to more sophisticated lenses that can superimpose computer-generated high-resolution color graphics on a user's real field of vision."

For now, Parviz mentions that single pixel visual cues for gamers and the hearing impaired are already quite possible with the lens prototypes. The group has also experimented with non-invasive biomonitoring including checking glucose levels for diabetics.

Some of the obvious challenges of building an augmented reality contact lens include:
1. The Need for Custom Parts: Regular circuitry and LEDs are incompatible with regular contact lenses. Every piece of this project must be fabricated from scratch.

2. Physical Constraints: The group must attempt to fit transistors, radio chips, antennas, diffusion resistors, LEDs and photodetectors onto a miniscule polymer disc. Additionally, the team is required to control lens position and light intensity relative to the pupil. And finally, because the lens is so close to the corneal surface, the group must project images away from the cornea using either micro-lenses or lasers.
3. User Safety: In addition to protecting the eye against chemicals, heat and toxins, the lens components must be semi-transparent in order for the wearer to view their surroundings.

"We already see a future in which the humble contact lens becomes a real platform, like the iPhone is today, with lots of developers contributing their ideas and inventions. As far as we're concerned, the possibilities extend as far as the eye can see." And you thought the iPhone SDK was a tough nut to crack.

For Parviz's complete seven page article, check out the IEEE Spectrum's Biomedical page.

Brain Health Tip #8

2009-09-05T16:07:00.000-04:00

Find a Smart Spouse

Did you know that the intelligence of your spouse will affect YOUR intelligence?

Believe it or not, finding the right spouse could make you smarter.

Researchers Warner Schaie and Sherry Willis have done a great deal of work in the areas of aging and cognition, and have reported the following in their publication Mind Alert:

“In our study, we followed a number of married couples over a long period of time. It turns out that married couples’ intellectual performance converges over time: The spouse with lower cognitive functioning early in the marriage moves in the direction of the higher-functioning spouse, cognitively speaking. So the bottom line is that you should marry someone who’s smarter than you are.”

Your spouse can be good (or bad) for your mental health!

This brain health tip courtesy of Luminosity.com

Brain Health Tip #7

2009-09-04T16:04:00.001-04:00

Use Your Attention Wisely

You can increase your attentiveness and what you select to attend to by developing the prefrontal cortex. The prefrontal cortex is the most evolved part of the brain and is responsible for judgment, attention span, concentration and critical thinking. Because it can be trained through activities requiring sustained attention such as reading, a more developed and utilized prefrontal cortex can better ignore the distractions that zap time from our days, thereby decreasing feelings of being overwhelmed.

To this point, Winifred Gallagher, author of Rapt: Attention and the Focused Life, breaks the myth of multitasking: "People don’t understand that attention is a finite resource, like money,” she said. “Do you want to invest your cognitive cash on endless Twittering or Net surfing or couch potatoing?" Probably not.

So turn your phone off, close your email, and invest in some ear plugs to find space in your life for prefrontal cortex development. Focus on what is important to you!

This tip courtesy of Luminosity.com

Bionic brain chips could overcome paralysis

2009-09-03T10:09:00.002-04:00

A MONKEY sits on a bench, wires running from its head and wrist into a small box of electronics. At first the wrist lies limp, but within 10 minutes the monkey begins to flex its muscles and move its hand from side to side. The movements are clumsy, but they are enough to justify a rewarding slug of juice. After all, it shouldn't be able to move its wrist at all.

A nerve connection in the monkey's upper arm had previously been blocked with an anaesthetic that prevented signals travelling from its brain to its wrist, leaving the muscles temporarily paralysed. The monkey was only able to move its arm because the wires and the black box bypassed the broken link.

The monkey was in Eberhard Fetz's lab at the University of Washington in Seattle. The experiment, performed last year, was the first demonstration of a new treatment that might one day cure paralysis, which is typically caused by a broken connection in the spinal cord. Though much work has focused on using stem cells to regrow damaged nerve fibres, some researchers believe that an electronic bypass like this is equally viable.

The idea is to implant electronic chips in the relevant regions of the brain to record neural activity. Then a decoder deciphers the neural chatter, often from thousands of neurons, to figure out what the brain wants the body to do. These messages must then be relayed - ideally wirelessly - to electrodes that deliver a pulse of electricity to stimulate the muscles into action. Such "brain chips" are already restoring hearing to the deaf and vision to the blind, and helping to stave off epileptic fits, so the idea isn't as far-fetched as it might sound (see "Bionic medicine").

Every step of progress in tackling paralysis has been hard won. One of the early demonstrations that it may be possible emerged in 2003, when José Carmena, then at Duke University in Durham, North Carolina, successfully created an interface between brain and machine that allowed his lab monkeys to play a computer game using only their minds.

To gain a juice reward, the monkeys had to move a cursor - initially with a joystick - to hit a target on the computer screen. Beforehand, Carmena and his colleagues had implanted several chips throughout the parietal and frontal lobes of the monkeys' brains - regions known to plan and control movement. Each chip held up to 64 electrodes, which recorded the firing of the surrounding neurons as the monkeys manipulated the joystick.

Once the system had successfully decoded the chatter from the monkeys' neurons, the program stopped responding to the joystick's movement altogether and relied solely on the monkeys' thoughts to control the cursor. Eventually even the animals worked this out and stopped holding the joysticks as they completed the task (PLoS Biology, vol 1, p 42).

Manipulating a cursor on a computer screen is one thing, but whether such brain chips could translate the more complicated tasks of daily life remained an open question until 2004, when John Donoghue and colleagues from Cyberkinetics in Providence, Rhode Island, implanted a 100-electrode chip in the brain of a 25-year-old man known as MN, who had been left paralysed from the neck down by a knife wound.

Over the subsequent nine months, MN successfully used this BrainGate chip to open emails, operate a television and even control a robotic arm (Nature, vol 442, p 164). It was a promising step, but the technology was far from perfect. "Although BrainGate1 worked well in many ways, at times the control was not satisfactory," says Donoghue. And by the end of the trial, fluids from the brain had degraded the chip. The team are now solving these problems, and earlier this year announced the start of a clinical trial for an improved version of the chip.

With a chip implanted in his brain, a paralysed man was able to open emails, operate the TV and even control a robotic arm

The ultimate hope for many paralysed people, of course, is to regain movement in their own limbs. Until Fetz's experiment last year, no one had successfully used an implant to bridge a broken connection between the brain and the body. Trials of functional electrical stimulation (FES), in which implanted electrodes directly stimulate muscles into action, had hinted that this might be possible. But these impulses had been activated by external triggers, such as a switch controlled by one of the patient's healthy limbs, and not directly by brain signals.

Not only did Fetz's work demonstrate that the electronics could descramble neural signals and relay appropriate instructions to the limbs using FES, he also showed that the brain makes the job easier than one might expect. Although the motor neurons that connected to the chip did not naturally control the wrist, in a short time they adapted to the task and controlled complex actions (Nature, vol 456, p 639). "All neurons could be used equally well for control regardless of their original association to movement," says team member Chet Moritz.

Read the rest of the original article at NewScientist.com

First Close Look At Stimulated Brain

2009-08-31T10:44:00.002-04:00

For over a century, scientists have been using electrical stimulation to explore and treat the human brain. The technique has helped identify regions responsible for specific neural functions—for instance, the motor cortex and pleasure center—and has been used to treat a variety of conditions from Parkinson's disease to depression. Yet no one has been able to see what actually happens at the cellular level when the brain is electrically prodded.

Now, with the aid of optical imaging technology, researchers in the lab of HMS neurobiology professor Clay Reid have taken the first look at this process. They found that the neural response to electrical currents isn't localized, as some had previously thought. That is, not all neurons immediately surrounding an electrode fire when a charge is delivered. Rather, a scattered and widely distributed set of neurons switch on. These findings, which will appear in the August 27 issue of Neuron, promise to end a longstanding debate about how neurons react to electrical stimulation.

Traditionally, observing neurons during electrical stimulation has been problematic. First author Mark Histed, a postdoctoral fellow in Reid's lab, explains, "When you are stimulating electrically you are using relatively high voltages, and those high voltages make it almost impossible to record the very small currents that neurons produce."

To sidestep this obstacle, Histed, Reid and postdoctoral fellow Vincent Bonin used a relatively new form of optical imaging called two-photon microscopy. The technique allowed them to track calcium levels in the neurons of mice as they were being exposed to electrical stimulation. When calcium levels increased, a chemical that had been introduced into the tissue brightened. Since calcium levels spike every time a neuron fires, the team could literally see the neurons flash each time they were activated. More importantly, they could monitor which neurons were being triggered.

According to Histed, these findings run counter to a long-standing hypothesis. "One prior theory was that at low currents, the neurons in a tiny ball around the electrode would activate, and if you increased the current, a larger ball would activate, but you would still only activate cells within that ball. What we showed was that, even at the lowest currents, you have cells very far away that are activated, so it's not just a tiny ball around the electrode tip that increases in size, but instead a very large, sparse pattern that fills in as the current is increased."

The researchers suspect that this sparsely distributed activation pattern results because it's really the axons—the long, thin fibers that transmit electrical signals in the nerve cells—that are being stimulated, not the cell bodies. To prove this, they moved the electrode tip 10 microns from the site of their first stimulations. That's a distance smaller than the width of just one nerve cell. Reid says, "you might guess that the same neurons would light up. But, in fact, the same number of neurons lit up, but they were entirely different neurons, and that really proved to us the hypothesis that we're exciting just a tiny little ball of neural processes, not neurons. We think we're exciting the axons in that 10 micron sphere."

Histed compares the neural mass to a box of unwound yo-yos. If you stick a pencil into that box, the tip of the pencil would touch only a few strings. Follow those strings all the way to their respective disks, and you would be "activating" only a few, scattered yo-yos within the knotted heap. Move the pencil tip just a quarter of an inch, and it touches a completely different group of strings, leading to an entirely different set of bodies.

The researchers believe that this study establishes optical imaging as a vital tool for any scientific and clinical research that involves electrical brain stimulation. Reid hopes that it will also "be very important in understanding, rationalizing, and designing neural prostheses." Such prostheses are already being used to cure deafness and to treat movement disorders, and Reid's lab has itself conducted research into the use of electrical stimulation to restore vision. This study, by shedding light on how electrical stimulation acts on the brain at the cellular level, could lead to the reinterpretation and refinement of earlier research in the field, and may help guide experiments.

This work was supported by NIH grants and by Microsoft Research.

Brain Health Tip #6

2009-08-29T20:15:00.001-04:00

5 Ways Pet Ownership Benefits the Brain

Pets can bring more to your life than joy and happiness. Recent studies have shown that animals can contribute to long-term mental health, too!

Psychologically, animals have been shown to:

1-Increase sympathy and social interaction.

2-Combat loneliness.

3-Soothe some brain diseases like Alzheimer's and autism, by providing memory and emotional stimulation.

Physically, animals' requirements will often get their owners to:

4-Leave the house or start a walk -- physical exercise is good for the brain!

5-Ease stress to the extent that their presence can even speed recovery from surgery/trauma.

So if you've been looking for another reason to add a new pet to your family, you can now say that it's good for your brain health, too!

This tip courtesy of Luminosity.com

Turning back the clock: Fasting prolongs reproductive life span

2009-08-28T12:50:00.002-04:00

Scientific dogma has long asserted that females are born with their entire lifetime's supply of eggs, and once they're gone, they're gone. New findings by researchers at Fred Hutchinson Cancer Research Center, published online Aug. 27 in Science, suggest that in nematode worms, at least, this does not hold true. This may also be further evidence that reduction caloric intake will slow aging.

Read original article at Physorg.com

Brain Health Tip #5

2009-08-26T10:36:00.002-04:00

How Noise Affects Cognition and Mood

We subject ourselves to 'acoustic startle response' each morning we're roused by the unpleasant sounds from an alarm clock. This abuse can, in the long run, induce cardiovascular and digestive distress.

We also become mentally combative when we're pummeled with noise, such that the World Health Organization notes aggressiveness as a health risk of noise. Additionally, other cognitive functions are sacrificed in the presence of noise-induced anger.

Psychologist Arline Bronzaft's research has shown that, in the case of a school located next to a train track, students' performance is hampered by noise. On the quieter side of the school, students performed at a reading level higher than the students on the train side. When measures were taken to insulate the noise-affected students, their performance evened out.

Beyond this, stroke victims have also been reported to have increased visual awareness when listening to preferred music, and surgery patients have reported less pain while listening to nature sounds.

The takeaway? Take measures to calm your mind and body by using more soothing sounds to wake you up in the morning. And whenever possible, try drowning out noise by listening to something pleasant. Your brain will thank you!

This brain health tip is courtesy of Luminosity.com

New Measure of Human Brain Processing Speed

2009-08-25T11:12:00.001-04:00

Tues, august 25,2009

A new way to analyze human reaction times shows that the brain processes data no faster than 60 bits per second.

For more than a century, psychologists have used reaction time as a window into the brain. The thinking is that information processing takes time, so the average time taken to begin or complete a task reflects the duration of the cognitive processes involved in it.

For example, a typical reaction time experiment might ask a subject to classify a sequence of letters as a word or a nonword, by pressing a button. This kind of experiment is called a visual lexical decision task.

This information-centric approach is clearly ripe for an information-theoretic treatment. And sure enough, no sooner had Shannon published his theory of information in the 1940s, psychologists began to apply it to the exchange of information between the environment and the brain that goes on during reaction time experiments.

Their approach eventually lead to Hick's Law, one of the few laws of experimental psychology. It states that the time it takes to make a choice is linearly related to the entropy of the possible alternatives. The results from various reaction time experiments seem to show that this is the case. Although one by-product of this approach is that the results are intimately linked to the type of experiment used to measure the reaction time. And that makes each study peculiarly vulnerable to the idiosyncracies of the experimental approach.

Today, Fermín Moscoso Del Prado Martín from the Universite de Provence in France proposes a new way to study reaction times by analysing the entropy of their distribution, rather in the manner of thermodynamics

The entropy is an estimate of the amount of information needed to specify the state of the system.

Martin says the the entropy of the distribution of reaction times is independent of the type of experiment and so provides a better measure of the cognitive processes involved. That's important, not least because it provides a way to more easily compare the results from different types of experiment.

Martin uses his method to determine how much information the brain can process during lexical decision tasks. The answer? No more than about 60 bits per second. Of course, this is not the information processing capacity of the entire brain but one measure of the input/output capacity during a specific task.

Martin goes on to analyse the data from various types of reaction time experiment, in particular to determine whether information processing speed is constant during a particular task, as implied by Hick's law. Martin reckons it isn't.

"This finding suggests an adaptive system where the processing load is dynamically adjusted to the task demands," he says. That makes sense. It seems crazy to assume that the brain carries on processing data at the same rate regardless of the complexity of task at hand.

But this has an important implication: that the linearity of Hick's law doesn't always apply. So Hick's law will need some kind of modification to cope with this non-linearity.

Just how to re-write one of the basic laws of behavioural psychology isn't clear yet. But it's sure to involve a very different way of looking at the brain form when it was formulated.

Ref: arxiv.org/abs/0908.3170: The Thermodynamics of Human Reaction Times
at the Technology review by MIT

Researchers develop 'brain-reading' methods

2009-08-23T03:39:00.001-04:00

It is widely known that the brain perceives information before it reaches a person's awareness. But until now, there was little way to determine what specific mental tasks were taking place prior to the point of conscious awareness.

That has changed with the findings of scientists at Rutgers University in Newark and the University of California, Los Angeles who have developed a highly accurate way to peer into the brain to uncover a person's mental state and what sort of information is being processed before it reaches awareness. With this new window into the brain, scientists now also are provided with the means of developing a more accurate model of the inner functions of the brain.

As reported in a forthcoming (Oct. 2009) issue of Psychological Science, the findings obtained by Stephen José Hanson, psychology professor at Rutgers; Russell A. Poldrack, professor at UCLA, and Yaroslav Halchenko, (now a post-doctoral student at Dartmouth College), have provided direct evidence that a person's mental state can be predicted with a high degree of accuracy through functional magnetic resonance imaging (fMRI). The research also suggests that a more comprehensive approach is needed for mapping brain activity and that the widely held belief that localized areas of the brain are responsible for specific mental functions is misleading and incorrect.

The research was funded with grants from the U.S. Office of Naval Research, the James S. McDonnell Foundation and National Science Foundation. The McDonnell Foundation recently awarded Hanson another $1 million for ongoing studies in this area.

Over the last several years, much of neuroimaging has focused on pinpointing areas of the brain that are uniquely responsible for specific mental functions, such as learning, memory, fear and love. But this latest research shows that the brain is more complex than that simple model. In their analysis of global brain activity, the researchers found that different processing tasks have their own distinct pattern of neural connections stretching across the brain, similar to the fingerprints that distinctively identify each of us. Rather than being a static pattern, however, the brain is able to arrange and rearrange the connections based on the mental task being undertaken.

"You can't just pinpoint a specific area of the brain, for example, and say that is the area responsible for our concept of self or that part is the source of our morality," says Hanson. "It turns out the brain is much more complex and flexible than that. It has the ability to rearrange neural connections for different functions. By examining the pattern of neural connections, you can predict with a high degree of accuracy what mental processing task a person is doing."

The findings open up the possibility of categorizing a multitude of mental tasks with their unique pattern of neural circuitry and also represent a potential first, early step in developing a means for identifying higher-level mental functions, such as 'lying' or abstract reasoning. They potentially also could pave the way for earlier diagnosis and better treatment of mental disorders, such as autism and schizophrenia, by offering a means for identifying very subtle abnormalities in brain activity and synchrony.

The research showing that specific mental functions do not correspond directly with certain brain areas but rather a unique pattern of neural connections also provides a more accurate direction for mapping the effective connectivity of the brain. Known as the Connectome Project, the goal of researchers involved in that work is to provide a complete map of the neural circuitry of the central nervous system.

"What our research shows is that if you want to understand human cognitive function, you need to look at system-wide behavior across the entire brain," explains Hanson. "You can't do it by looking at single cells or areas. You need to look at many areas of the brain to even understand the simplest of functions."

The study involved 130 participants, each of whom performed a different mental task, ranging from reading, to memorizing a list, to making complex decisions about whether to take monetary risks, while being scanned using fMRI. The researches were able to identify which of eight tasks participants were involved in with more than 80-percent accuracy by analyzing the participants' fMRI data against classifications developed from the fMRIs of other individuals. The researchers also were able to identify what class of objects (faces, houses, animals, etc.) a person was viewing before he or she could report that information by analyzing the pattern of brain activity at the back of the brain where information is processed and then conveyed towards the frontal regions associated with awareness.

"It's the same principle experienced during a car accident. The car accident actually happens tens of a milliseconds before you are aware you have actually been hit," explains Hanson. "By looking at the back of the brain, we can 'read out,' for example, that a person is looking at dogs and cats before they actually know they are looking at a dog or a cat."

Unlike most research that has focused on specific areas of the brain, Hanson and his team looked at the pattern of activity across a half million points in the brain. Interestingly, the patterns of neural networks involved in each of the eight tasks on the surface appear very similar. The reason, Hanson explains, is that various mental functions tend to draw on many of the same processes. For example, memorizing a list of words that include the word dog is likely to draw up a memory of a pet, the same as reading a story about a dog would. Using machine learning techniques (a support vector machine), capable of analyzing and categorizing large amounts of data, the researchers were able to identify those slight differences that allowed them to predict the specific mental function of the participants and what information they would report back.

"It's like looking at two patterns of identical flower arrangements," says Hanson. "They each may have the same flowers but they will not be arranged exactly in the same manner, consequently leading to slight differences in the overall pattern. Using the pattern analysis methods we have developed, there are clues that can be detected and pulled out."

As part of their continuing research, Hanson and his team plan to develop a system for identifying neural connectivity abnormalities to assist with the study of such mental disorders as attention-deficit hyperactivity and autism and to produce a handbook for many of the new tools used for pattern analysis and the classification of mental states based on neuroimaging data.

Source: Rutgers University (news : web)
Physorg.com

Artificial brain '10 years away'

2009-08-21T12:07:00.001-04:00

Professor Markram said he would send a hologram to talk at TED in 10 years

A detailed, functional artificial human brain can be built within the next 10 years, a leading scientist has claimed.

Henry Markram, director of the Blue Brain Project, has already simulated elements of a rat brain.

He told the TED Global conference in Oxford that a synthetic human brain would be of particular use finding treatments for mental illnesses.

Around two billion people are thought to suffer some kind of brain impairment, he said.

"It is not impossible to build a human brain and we can do it in 10 years," he said.

"And if we do succeed, we will send a hologram to TED to talk."

'Shared fabric'

The Blue Brain project at Swizerland's EPFL (École Polytechnique Fédérale de Lausanne) was launched in 2005 and aims to reverse engineer the mammalian brain from laboratory data.

In particular, his team has focused on the neocortical column - repetitive units of the mammalian brain known as the neocortex.

The team are trying to reverse engineer the brain

"It's a new brain," he explained. "The mammals needed it because they had to cope with parenthood, social interactions complex cognitive functions.

"It was so successful an evolution from mouse to man it expanded about a thousand fold in terms of the numbers of units to produce this almost frightening organ."

And that evolution continues, he said. "It is evolving at an enormous speed."

Over the last 15 years, Professor Markram and his team have picked apart the structure of the neocortical column.

"It's a bit like going and cataloguing a bit of the rainforest - how many trees does it have, what shape are the trees, how many of each type of tree do we have, what is the position of the trees," he said.

"But it is a bit more than cataloguing because you have to describe and discover all the rules of communication, the rules of connectivity."

The project now has a software model of "tens of thousands" of neurons - each one of which is different - which has allowed them to digitally construct an artificial neocortical column.

Although each neuron is unique, the team has found the patterns of circuitry in different brains have common patterns.

"Even though your brain may be smaller, bigger, may have different morphologies of neurons - we do actually share the same fabric," he said.

"And we think this is species specific, which could explain why we can't communicate across species."

World view

To make the model come alive, the team feeds the models and a few algorithms into a supercomputer.

"You need one laptop to do all the calculations for one neuron," he said. "So you need ten thousand laptops."

The research could give insights into brain disease

Instead, he uses an IBM Blue Gene machine with 10,000 processors.

Simulations have started to give the researchers clues about how the brain works.

For example, they can show the brain a picture - say, of a flower - and follow the electrical activity in the machine.

"You excite the system and it actually creates its own representation," he said.

Ultimately, the aim would be to extract that representation and project it so that researchers could see directly how a brain perceives the world.

But as well as advancing neuroscience and philosophy, the Blue Brain project has other practical applications.

For example, by pooling all the world's neuroscience data on animals - to create a "Noah's Ark", researchers may be able to build animal models.

We cannot keep on doing animal experiments forever," said Professor Markram.

It may also give researchers new insights into diseases of the brain.

"There are two billion people on the planet affected by mental disorder," he told the audience.

The project may give insights into new treatments, he said.

The TED Global conference runs from 21 to 24 July in Oxford, UK.

Original article by Jonathan Fildes for the technology reporter on BBC news

Tests Begin on Drugs That May Slow Aging

2009-08-20T14:39:00.004-04:00

Tests Begin on Drugs That May Slow Aging

August 17, 2009

It may be the ultimate free lunch — how to reap all the advantages of a calorically restricted diet, including freedom from disease and an extended healthy life span, without eating one fewer calorie. Just take a drug that tricks the body into thinking it’s on such a diet.

VIEW As evolutionary biologists see it, each species' life span is adapted to the nature of its environment. The maximum lifespan of bats, for example, is 3.5 times greater than flightless mammals of the same size, the research shows.

It sounds too good to be true, and maybe it is. Yet such drugs are now in clinical trials. Even if they should fail, as most candidate drugs do, their development represents a new optimism among research biologists that aging is not immutable, that the body has resources that can be mobilized into resisting disease and averting the adversities of old age.

This optimism, however, is not fully shared. Evolutionary biologists, the experts on the theory of aging, have strong reasons to suppose that human life span cannot be altered in any quick and easy way. But they have been confounded by experiments with small laboratory animals, like roundworms, fruit flies and mice. In all these species, the change of single genes has brought noticeable increases in life span.

With theorists’ and their gloomy predictions cast in the shade, at least for the time being, experimental biologists are pushing confidently into the tangle of linkages that evolution has woven among food intake, fertility and life span. “My rule of thumb is to ignore the evolutionary biologists — they’re constantly telling you what you can’t think,” Gary Ruvkun of the Massachusetts General Hospital remarked this June after making an unusual discovery about longevity.

Excitement among researchers on aging has picked up in the last few years with the apparent convergence of two lines of inquiry: single gene changes and the diet known as caloric restriction.

In caloric restriction, mice are kept on a diet that is healthy but has 30 percent fewer calories than a normal diet. The mice live 30 or 40 percent longer than usual with the only evident penalty being that they are less fertile.

People find it almost impossible to maintain such a diet, so this recipe for longevity remained a scientific curiosity for many decades. Then came the discovery of the single gene changes, many of which are involved in the body’s regulation of growth, energy metabolism and reproduction. The single gene changes thus seem to be pointing to the same biochemical pathways through which caloric restriction extends life span.

If biologists could only identify these pathways, it might be possible to develop drugs that would trigger them. Such drugs could in principle have far-reaching effects. Mice on caloric restriction seem protected from degenerative disease, which may be why they live longer. A single drug that protected against some or all the degenerative diseases of aging would enable people to enjoy more healthy years, a great benefit in itself, even if it did not extend life span.

The leading candidates for such a role are drugs called sirtuin activators, which may well be mimicking caloric restriction, in whole or in part. The chief such drug is resveratrol, a minor ingredient of grapes and red wine. Sirtris Pharmaceuticals, of Cambridge, Mass., is now conducting clinical trials of resveratrol, in a special formulation, and of small-molecule drugs that also activate sirtuin but can be given in much lower doses. The resveratrol formulation and one of the small chemicals have passed safety tests and are now being tested against diabetes and other diseases. The Food and Drug Administration does not approve drugs to delay aging, because aging in its view is not a disease.

The sirtuin activators have a strong scientific pedigree. They emerged as the surprising outcome of a quest begun in 1991 by Leonard P. Guarente of M.I.T. to look for genes that might prolong life span in yeast, a single-cell organism. Working with David A. Sinclair, now at Harvard Medical School, he discovered such a gene, one called sir-2. People and mice turned out to have equivalent genes, called sirt genes, that produce proteins called sirtuins.

Dr. Guarente then found that the sirtuins can detect the energy reserves in a cell and are activated when reserves are low, just what would be needed for a protein that mediates the effects of caloric restriction. Dr. Sinclair and colleagues screened a number of chemicals for their ability to activate sirtuin, and resveratrol landed at the top of the list. The chemical was already known as the suspected cause of the French paradox, the fact that the French eat a high fat diet without penalty to their longevity.

The two researchers and their colleagues thus argued that caloric restriction works by activating sirtuins, and so drugs that activate sirtuins should offer the same health benefits.

In 2004 Dr. Sinclair co-founded Sirtris with Christoph Westphal, a scientific entrepreneur. Helped by growing interest in the sirtuin story, Dr. Westphal was able to sell the company last year to GlaxoSmithKline for $720 million.

Dr. Sinclair says that “the results from the Sirtris compounds are promising and will be submitted for publication in coming months.”

But despite the high promise and strong scientific foundation of the sirtuin approach, it has yet to be proved that Sirtris’s drugs will work. The first of many questions is that of whether caloric restriction applies at all to people.

Two experts on aging, Jan Vijg of the Albert Einstein College of Medicine and Judith Campisi of the Lawrence Berkeley National Laboratory, argued recently in Nature that the whole phenomenon of caloric restriction may be a misleading result unwittingly produced in laboratory mice. The mice are selected for quick breeding and fed on rich diets. A low-calorie diet could be much closer to the diet that mice are adapted to in the wild, and therefore it could extend life simply because it is much healthier for them.

“Life extension in model organisms may be an artifact to some extent,” they wrote. To the extent caloric restriction works at all, it may have a bigger impact in short-lived organisms that do not have to worry about cancer than in humans. Thus the hope of mimicking caloric restriction with drugs “may be an illusion,” they write.

To decide whether life extension by caloric restriction is an artifact of mice in captivity, why not try it on wild mice? Just such an experiment has been done by Steven N. Austad of the University of Texas Health Science Center. Dr. Austad reported that caloric restriction did not extend the average life span of wild mice, suggesting the diet’s benefits are indeed an artifact of mice in captivity. But others interpret his results differently. Richard A. Miller of the University of Michigan, says the maximum life span of the wild mice was extended, and so the experiment was a success for caloric restriction.

Laboratory mice are very inbred, and researchers can get different results depending on the breed they use. To put the mouse data on a firmer footing, the National Institute on Aging has set up a program to test substances in three labs simultaneously. Its first round of candidate agents for reversing aging include green tea extract and two doses of resveratrol.

The resveratrol tests are still under way, but last month the results with another substance, the antifungal drug rapamycin, were published. Rapamycin was found to extend mice’s lives significantly even though by accident the mice were already the equivalent of 60 years old when the experiment started.

Rapamycin has nothing to do with caloric restriction, so far as is known, but the study provided striking proof that a chemical can extend life span.

Another result, directly related to the caloric restriction approach, emerged last month from a long-awaited study of rhesus monkeys kept on such a diet. The research was led by Richard Weindruch of the University of Wisconsin. As fellow primates, the monkeys are the best possible guide to whether the mouse results will apply in people. And the answer they gave was ambiguous.

The monkeys who had spent 20 years on caloric restriction were in better health than their normally fed counterparts, and suffered less diabetes, cancer and heart disease, apparently confirming that caloric restriction holds off the degenerative diseases of aging in primates as well as rodents.

But as for life span, the diet extended life significantly only if the researchers excluded deaths that were apparently unrelated to aging, such as under the anesthesia necessary to take blood samples. When all deaths were counted, life span was not significantly extended.

Some researchers think it is perfectly valid to ignore such deaths. Others note that in mouse studies one just counts the numbers of dead mice without asking what they died of, and the same procedure should be followed with monkeys, since one cannot be sure if a death under anesthesia might have been age related.

With the rapamycin and rhesus monkey results, Dr. Sinclair said, “We have more weight on the side of people who think it’s going to be possible.” He stressed the ability of both caloric restriction and sirtuin-activating drugs to postpone the many diseases of aging, at least in mice. To have one drug that postponed many degenerative diseases in people would be a significant advance, he said, even without any increase in longevity.

People may live so long already that no drug could make much of a difference. Probably because of reductions in infant mortality and other types of disease, human life expectancy in developed countries has been on a remarkable, unbroken upward trend for the last 160 years. Female life expectancy at birth rose from 45 years in 1840 to 85 years in 2000.

An important difference among experts on aging is whether there is an intrinsic rate of aging. Supposing there were cures for all diseases, what would one die of, if one died at all? Dr. Vijg and Dr. Campisi believe there is a steady buildup of damage to DNA and to proteins like the collagen and elastin fibers that knit the body together. Damage to DNA means that the regulation of genes gets less precise, and this regulatory drift disrupts the stem cells that repair each tissue. Even if all disease could be treated, it is not clear that anything could overcome intrinsic aging.

Dr. Miller, on the other hand, believes no clear distinction can be made between disease and other frailties of aging. “Anything a doctor can charge for we call disease, but wrinkled skin, white hair or not feeling good in the morning, these we don’t call disease,” he said.

He thinks that the idea of intrinsic aging is not well defined and that contrary to the theories of the evolutionary biologists, there may be simple ways to intervene in the aging process.

In the view of evolutionary biologists, the life span of each species is adapted to the nature of its environment. Mice live at most a year in the wild because owls, cats and freezing to death are such frequent hazards. Mice with genes that allow longer life can rarely be favored by natural selection. Rather, the mice that leave the most progeny are those that devote resources to breeding at as early an age as possible.

According to this theory, if mice had wings and could escape their usual predators, natural selection ought to favor longer life. And indeed the maximum life span of bats is 3.5 times greater than flightless mammals of the same size, according to research by Gerald S. Wilkinson of the University of Maryland.

In this view, cells are so robust that they do not limit life span. Instead the problem, especially for longer-lived species, is to keep them under control lest they cause cancer. Cells have not blocked the evolution of extremely long life spans, like that of the bristlecone pine, which lives 5,000 years, or certain deep sea corals, whose age has been found to exceed 4,000 years.

Some species seem to be imperishable. A tiny freshwater animal known as a hydra can regenerate itself from almost any part of its body, apparently because it makes no distinction between its germ cells and its ordinary body cells. In people the germ cells, the egg and sperm, do not age; babies are born equally young, whatever the age of their parents. The genesis of aging was the division of labor in the first multicellular animals between the germ cells and the body cells.

That division put the role of maintaining the species on the germ cells and left the body cells free to become specialized, like neurons or skin cells. But in doing so the body cells made themselves disposable. The reason we die, in the view of Thomas Kirkwood, an expert on the theory of aging, is that constant effort is required to keep the body cells going. “This, in the long run, is unwarranted — in terms of natural selection, there are more important things to do,” he writes.

All that seems clear about life span is that it is not fixed. And if it is not fixed, there may indeed be ways to extend it.

Article by Nicholas Wade for New York Times

Fatty Foods Affect Memory and Exercise

2009-08-18T12:30:00.001-04:00

New York Times, Aug. 13, 2009

Eating fatty food appears to take an almost immediate toll on both short-term memory and exercise performance, according to new research on rats and people.

Other studies have suggested that long-term consumption of a high-fat diet is associated with weight gain, heart disease and declines in cognitive function. But the new research shows how indulging in fatty foods over the course of a few days can affect the brain and body long before the extra pounds show up.

To determine the effect of a fatty diet on memory and muscle performance, researchers studied 32 rats that were fed low-fat rat chow and trained for two months to complete a challenging maze. The maze included eight different paths that ended with a treat of sweetened condensed milk. The goal was for the rat to find each treat without doubling back into a corridor where it had already been. The maze was wiped down with alcohol, so the rat had to rely on memory rather than sense of smell.

Read original article --->here<---

Immortality improves cell reprogramming

2009-08-12T19:39:00.002-04:00

Nature News Aug. 9, 2009

Specialized adult cells made 'immortal' through the blockade of an antitumour pathway can be turned into stem-like cells quickly and efficiently.

The findings — which should make it easier to generate patient-specific cells from any tissue type, including certain diseased cells that have proved difficult to transform — suggest that cellular reprogramming and cancer formation are inextricably linked.

Read rest of article here

Avoid Heart Disease by Boosting Your Mood

2009-08-09T22:11:00.000-04:00

By Dr. Michael Cutler • Aug 5th, 2009 • Category: Dr. Cutler's True Health Blog Archive, General Health, Health Articles, Heart Health

Unfortunately, at some point in our lives, we’ve all experienced the sting of loneliness. It can make you miserable, and depending on the depth of your despair, it can be devastating. Loneliness carries with it risks for heart disease, cancer, suppressed immune function, depression, premature aging and even a shortened life span.

Psychologist and biologist Joan Borysenko said, “To be isolated is the greatest tragedy for a human being and the most generic form of stress.” Not only can it rob you of your joy, it can literally set you up for serious illnesses that can take your life.

Check out the following studies…

Go here for rest of article

Scientists Program Blood Stem Cells To Become Vision Cells

2009-08-05T22:48:00.001-04:00

ScienceDaily Aug. 3, 2009

University of Florida researchers
have programmed bone marrow stem
cells to build retinal pigment
epithelial cells by mimicking the
body's natural signaling channels
with chemicals instead of genetic...

Read original article--->here<----

Brain Health Tip #4

2009-08-04T22:37:00.002-04:00

How stress affects decision making

While it's been documented for some time that men take more risks than women (and, thus, are more likely to die violently or have addictive behaviors), a recent study indicates that this gap widens even further when stress is introduced.

When stress indicators as measured by cortisol levels were higher in women, their decision making was less risky than than their control group. Men, on the other hand, made more risky decisions when stressed than their control group did.

To test decision making under stress, participants' hands were placed in ice water while they performed a gambling game involving blowing up a simulated balloon on a computer screen. Points were accumulated with each pump of the balloon, but each pump also increased the risk of the balloon popping, resulting in a loss of all points.

The lesson here? Try to be aware of your gendered inclinations when you feel stressed out, so that you make the most responsible (men!) or effective (ladies!) decision. Consider what you'd normally do, and come up with a plan of action rather than react unthinkingly.

This article is curteosy of luminosity.com

Stats favor five-year prostate survivors

2009-07-08T07:32:00.001-04:00

U.S. researchers say prostate cancer patients disease-free after five years will likely be disease-free after 10 years.

The study of prostate cancer patients receiving brachytherapy, published in the International Journal of Radiation Oncology*Biology*Physics, finds cancer recurrences at 10 years unlikely in those who were deemed disease free at five years.

Brachytherapy is either the temporary or permanent placement of radioactive sources in or just next to a tumor.

"Our data have indicated that improvements in treatment are continuing and that these will continue to have an effect on prostate brachytherapy data for years to come," lead author Dr. Richard Stock of The Mount Sinai Medical Center in New York says in a statement.

"Late failure rates will continue to decrease, making prostate brachytherapy alone and combined with hormonal therapy and/or external beam radiation therapy an increasingly attractive treatment option."

The study followed 742 prostate cancer patients treated with brachytherapy alone, brachytherapy and hormonal therapy, or combined brachytherapy and external beam radiotherapy from 1991 to 2002.

None of these patients had recurrences during their first five years post-treatment. Prostate-specific antigen level taken at five years was an indicator of how well a patient would do in the future and the overall chance of being cancer free at 10 years was 97 percent, the study said.

Article courtesy of united press

Citrus relieves asthma

2009-07-07T08:16:00.006-04:00

Its a funny thing when you have had asthma for the better part of 13 years and have been to numerous asthma experts all of which only prescribe you a generalized inhaler and none of which can really tell you the cause, cure or ways to really protect yourself against getting it. Then suddenly you read a casual article on the net that citrus relieves asthma and you have something of an answer.

Some people think that because they didn't get it as a child they will never get it. The reality is that you CAN get it at any age. One of the biggest factors is genetics which gives you 25% better chance at getting it if your parents had allergies. other cause can be from your environment(eg.dust mites, which are in virtually everyone's house and pollen).

Alas there is hope. you may still be able to reduce damage cause by frequent asthma attacks. Duh -Duh -DA-- DAAAAA. Its citrus to the rescue.

Pretty much all citrus fruits such as grapefruit,oranges,lemons,limes helps reduce your risk of getting asthma. Its thought that the Vitamin C in citrus fruits facilitates the breathe easier effects. Also by eating these fruits you'll get a natural boost of antioxidants that are well documented in having anti aging properties

Other more commonly known recommendations usually made by asthma specialists include:

avoid dust mite waste. You can get a pillow casing to cover your pillow of as least 1 micron. Also wash your pillow cases and bed sheets at least weekly. Ive gone one step further myself and purchased a casing for my mattress as well.
The obvious one is to quit smoking ASAP
avoid high pollen count days. You can usually get information about this from your local weather station or on the net.(the weather network is great for this). I know this is a tough one but if you reduce your outdoor exposure at peak times in the day it may be worth the effort.
the other obvious one is to avoid any kind of air pollution like from cars. Roll up your window if you are in traffic

I know some of these recommendations will make your wallet a little lighter but I truly believe that the best investment you can make is in your health

The omega point- when life engulfs the universe

2009-06-28T08:00:00.006-04:00

I love to listen to controversial theories especially from Frank J. Tipler. I first read his work back in 1999's "The physics of immortality" in which he talks about the omega point being a mechanism for immortality and resurrection in which he believes will come from a super computer intelligence that he identifies with god.

He explains that "life is basically computing" in the documentary Technocalyps. He says that we will explore the universe through a form of virtual humanism. The universe will be converted into one giant cosmic computer network that will be all knowing, self sufficient.

According to the law of gravitation the universe will not keep expanding and is slowing down then it will contract again and evolves into the omega point which is beyond space and time. This omega point will be omnipotent, omnipresent, and all knowing thus is it god. This god network will resurrect us again. he belives that god goes back in our time and give us clues on how to create him back into the omega point.

A review in the well respected journal "NATURE" by gerorge ellis stated that it is:
"a masterpiece of pseudoscience ... the product of a fertile and creative imagination unhampered by the normal constraints of scientific and philosophical discipline". Pseudoscience it may be but still very entertaining and original pseudoscience.

In Tipler's new 2007 book "The physics of christianity" he weaves the idea of the omega point's theory as being important to christianity and that the omega point is the Judeo-christian god.
Personally i thought he went way over board in this book in trying to bridge the gap between science and religion, but in the end i wasn't too disappointed because it was entertaining and original.

If you'd like more information you can check out Frank Tipler's website -->HERE<--
If you'd like to check out his books at amazon go -->HERE<--