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Forever in your prime

Anything I find interesting about how to slow, prevent, and reverse aging.

Monday, April 06, 2009

Getting the word out

Look at the timeline for these articles:

2009-03-27: New Scientist

2009-01-01: Science Direct

2008-10-28: International Journal of Pharmaceutics

This is worrisome, as it is taking over 6 months for word of research to get out to the community.  I’m not sure if it’s better for people in the research field, I don’t know if they can find out who’s doing what faster than the lay-person can, but someone needs to get this info online for free much faster than is currently being done so people can co-ordinate.

Tuesday, June 03, 2008

Aging 2008 Symposium at UCLA

Methuselah Foundation Announces Aging 2008 at UCLA

Have you ever dreamed of climbing Mt. Everest – on your 125th birthday?

Los Angeles, CA (May 19, 2008) On Friday June 27th, leading scientists and thinkers in stem cell research and regenerative medicine will gather in Los Angeles at UCLA for Aging 2008 to explain how their work can combat human aging, and the sociological implications of developing rejuvenation therapies.

Aging 2008 is free, with advance registration required at http://www.mfoundation.org/Aging2008/.

Dr. Aubrey de Grey, chairman and chief science officer of the Methuselah Foundation, said "Our organization has raised over $10 million to crack open the logjams in longevity science. With the two-armed strategy of direct investments into key research projects, and a competitive prize to spur on scientists racing to break rejuvenation and longevity records in lab mice, the Foundation is actively accelerating the drive toward a future free of age-related degeneration." The Methuselah Foundation has been covered by 60 Minutes, Popular Science, The Wall Street Journal, and other top-flight media outlets.

The State of California is a frontrunner in regenerative medicine and stem cell research. On November 2, 2004, more than seven million Californians voted to pass Proposition 71, establishing the California Institute for Regenerative Medicine, and allocating $3 billion over ten years to fund stem cell research. Proposition 71 was a rare instance of voters directly authorizing funding for scientific research.

The speakers at Aging 2008 will argue that the near-term consequences of intense research into regenerative medicine could be the development of therapies that extend healthy human life by decades, even if the therapies are applied in middle age. Peter Thiel, president of Clarium Capital, initial investor in Facebook, and lead sponsor of Aging 2008, said, "The time has come to challenge the inevitability of aging. This forum will provide an excellent opportunity to look at the scientific barriers that must be overcome to substantially extend healthy human life, as well as the ethical implications of doing so."

Aging 2008 also serves as the free opening session for the technically focused Understanding Aging Conference, which will run at UCLA on June 28th and 29th.

What: Aging: The Disease, The Cure, The Implications, hosted by Methuselah Foundation
When:
Friday, June 27, 2008, Drinks 4pm, Presentations 5pm, Dinner 8pm
Where:
Royce Hall, 405 Hilgard Ave, Los Angeles, CA 90024
Who:

§ Dr. Bruce Ames, Professor of Biochemistry and Molecular Biology at UC Berkeley

§ G. Steven Burrill, Chairman of Pharmasset and Chairman of Campaign for Medical Research

§ Dr. Aubrey de Grey, Chairman and CSO of Methuselah Foundation and author of Ending Aging

§ Dr. William Haseltine, Chairman of Haseltine Global Health

§ Daniel Perry, Executive Director of Alliance for Aging Research

§ Bernard Siegel, Executive Director of Genetics Policy Institute

§ Dr. Gregory Stock, Director of Program on Medicine, Technology & Society at UCLA School of Medicine

§ Dr. Michael West, CEO of BioTime and Adjunct Professor of Bioengineering at UC Berkeley

About Methuselah Foundation

The Methuselah Foundation is a 501(c)(3) nonprofit organization dedicated to extending the healthy human lifespan. Founded in 2002 by entrepreneur David Gobel and gerontologist Dr. Aubrey de Grey, the Methuselah Foundation funds two major projects: the Mprize, a multimillion dollar research prize, and SENS, a detailed engineering plan to repair aging-related damage. Learn more at http://mfoundation.org.

Media Contact: Maria Entraigues, 310-242-3660, mailto:maria@mfoundation.org

Wednesday, February 06, 2008

Universal Flue Vaccine Tested Successfully

http://www.sciencedaily.com/releases/2008/01/080124185522.htm
ScienceDaily (Jan. 25, 2008)
The British-American biotech company Acambis reports the successful
conclusion of Phase I trials of the universal flu vaccine in humans. The
universal influenza vaccine has been pioneered by researchers from VIB and
Ghent University. This vaccine is intended to provide protection against all
'A' strains of the virus that causes human influenza, including pandemic
strains. Therefore, this vaccine will not need to be renewed annually.

Wednesday, January 16, 2008

10-Fold Life Span Extension Reported

01/14/08
Record longevity for baker's yeast suggests strategies for helping humans
live longer and healthier, says USC study leader Valter Longo.
By Carl Marziali

Longo's group next plans to further investigate life span extension in mice.

Photo/S. Peter LopezBiologists have created baker's yeast capable of living
to 800 in yeast years without apparent side effects.

The basic but important discovery, achieved through a combination of dietary
and genetic changes, brings science closer to controlling the survival and
health of the unit of all living systems: the cell.

"We're setting the foundation for reprogramming healthy life," said USC
study leader Valter Longo.

The study is scheduled to appear in the Jan. 25 issue of the journal PLoS
Genetics. A companion study, showing that the same genetic changes in yeast
reverse the course of an accelerated aging syndrome, appears in the Jan. 14
issue of the Journal of Cell Biology.

Longo's group put baker's yeast on a calorie-restricted diet and knocked out
two genes, RAS2 and SCH9, that promote aging in yeast and cancer in humans.

"We got a 10-fold life span extension that is, I think, the longest one that
has ever been achieved in any organism," Longo said. In 2005, the same
research group reported a five-fold life span extension in the journal Cell.
Normal yeast organisms live about a week.

"I would say 10-fold is pretty significant," said Anna McCormick, chief of
the genetics and cell biology branch at the National Institute on Aging and
Longo's program officer.

The NIA funds such research in the hope of extending healthy life span in
humans through the development of drugs that mimic the life-prolonging
techniques used by Longo and others, McCormick added.

Baker's yeast is one of the most studied and best understood organisms at
the molecular and genetic level. Remarkably, in light of its simplicity,
yeast has led to the discovery of some of the most important genes and
pathways regulating aging and disease in mice and other mammals.

A study recently published in Cell (Issue 130, pages 247-258, 2007) reported
that a mouse with a gene mutation first identified by Longo's group lived 30
percent longer than normal and also was protected against heart and bone
diseases without apparent side effects.

Longo's group next plans to further investigate life span extension in mice
and also is studying a human population in Ecuador with mutations analogous
to those described in yeast.

"People with two copies of the mutations have very small stature and other
defects," he said. "We are now identifying the relatives with only one copy
of the mutation, who are apparently normal. We hope that they will show a
reduced incidence of diseases and an extended life span."

Longo cautioned that, as in the Ecuador case, longevity mutations tend to
come with severe growth deficits and other health problems. Finding drugs to
extend the human life span without side effects will not be easy, he said.

An easier goal, Longo added, would be to use the knowledge gained about life
span "in a fairly limited way, to reprogram disease prevention."

In the study appearing in the Jan. 14 Journal of Cell Biology, Longo's group
developed a yeast model for human Werner/Bloom syndromes, incurable diseases
that prematurely age, increase cancer incidence and eventually kill their
victims.

The same mutations that play a central role in the 10-fold life span
extension reversed the premature aging process, the researchers found.

Longo suggested that although a very simple system was used in his studies,
existing drugs targeting analogous anti-aging pathways in humans -
specifically the pathway involving Insulin Growth Factor, or IGF-1 - should
be considered for testing on Werner/Bloom patients.

"Maybe it will do nothing, but having nothing else, I think it's certainly a
good thing to try," Longo said.

In the PLoS Genetics study, Longo's group identified a major overlap between
the genes previously implicated in life span regulation for yeast and
mammals and those involved in life span extension under calorie restriction.


"We identified three transcription factors . that are very important for the
effect of calorie restriction, but at the same time, we also showed that
it's not enough because even without these transcription factors, calorie
restriction can still extend life span a little bit," Longo said.

"So that means that we've identified a lot of the key players in the calorie
restriction effect but not all of them."

Calorie restriction - in practice, controlled starvation - has long been
shown to reduce disease and extend life span in species from yeast to mice.

Scientists believe that a nutrient shortage kicks organisms into a
maintenance mode, enabling them to redirect energy from growth and
reproduction into anti-aging systems until the time they can feed and breed
again.

Calorie restriction is now being tested by other researchers on primates and
even humans, Longo said.

Longo has been studying aging at the cellular level for 15 years and has
published articles in the nation's leading scientific journals. His
laboratory developed a simple and inexpensive method for measuring the true
chronological life span of yeast. Previously, scientists used the number of
a yeast cell's offspring as a proxy for its age.

The so-called replicative life span technique remains in use, and the NIA's
McCormick said that Longo's method was controversial at first. However, she
said, the scientific community now appears to accept its usefulness. She
said Longo's "stationary phase" method is particularly applicable to studies
of cells that do not divide for most of their life, such as those in the
brain or in muscle.

"Stationary phase I think of as normal cell survival," McCormick said. She
added that NIA funds both stationary phase and replicative life span
research.

Longo is the Albert L. and Madelyne G. Hanson Family Trust Associate
Professor in Gerontology with a joint appointment as associate professor of
biological sciences at USC College. A native of Italy, Longo came to the
United States to study jazz performance but switched his major to
biochemistry as an undergraduate at the University of North Texas. He earned
his Ph.D. in biochemistry from UCLA in 1997 and completed his postdoctoral
training in neurobiology at USC.

The studies were funded by NIA (part of the National Institutes on Health)
and the American Federation for Aging Research.

USC graduate students Min Wei and Paola Fabrizio were first authors on the
PLoS Genetics paper. USC graduate students Federica Madia and Cristina
Gattazzo were first authors on the Journal of Cell Biology paper.

The other members of Longo's group were USC graduate students Abdoulaye
Galbani, Jesse Smith, Christopher Nguyen, Selina Huey, Lucio Comai, Jia Hu,
Huanying Ge and Chao Cheng, USC computational biologist Lei Li, and William
Burhans and Martin Weinberger of the Roswell Park Cancer Institute in
Buffalo, N.Y.

Wednesday, December 26, 2007

Reversing skin aging

STANFORD, Calif. — Researchers at the Stanford University School of Medicine have reversed the effects of aging on the skin of mice, at least for a short period, by blocking the action of a single critical protein.The work could one day be useful in helping older people heal from an injury as quickly as they did when they were younger, said senior author Howard Chang, MD, PhD, assistant professor of dermatology. However, Chang and his colleagues warned their finding will likely be useful in short-term therapies in older people but not as a potential fountain of youth.The work backs up the theory that aging is the result of specific genetic changes rather than accumulated wear and tear, Chang said. What’s more, those genetic changes can be reversed even late in life.“The implication is that the aging process is plastic and potentially amenable to intervention,” Chang said. The results will be published in the Dec. 15 issue of the journal Genes and Development.The work came about thanks to existing data from experiments using microarrays, which detect the activity of all genes in a cell. In past experiments, researchers have found a large number of diverse genes that become either more active or less active in older people.Chang and graduate student Adam Adler, the study’s first author, searched through this existing data to see if those age-related genes had anything in common. It turned out that their activity gets dialed up or down with the help of the protein called NF-kappa-B.Chang said people had long known that NF-kappa-B winds its way into a cell’s nucleus to control which genes were active. What they didn’t know is that many of those genes regulated by the protein have a role in aging.Chang and Adler tested whether blocking the activity of NF-kappa-B in the skin of older mice for two weeks had a youthful effect. “We found a pretty striking reversal to that of the young skin,” Chang said.First they looked at the genetic changes resulting from blocking NF-kappa-B. After two weeks, the skin of 2-year-old mice had the same genes active as cells in the skin of newborn mice—a striking difference when compared with the skin of a normal 2-year-old mouse. The skin looked more youthful too. It was thicker and more cells appeared to be dividing, much like the skin of a younger mouse.Chang and Adler caution that their findings aren’t likely to be the source of the long-sought fountain of youth. That’s because they don’t know if the rejuvenating effects of NF-kappa-B are long-lasting. Also, the protein has roles in cancer, the immune system and a range of other functions throughout the body. Suppressing the protein on a long-term basis could very well result in cancers or other diseases that undermine its otherwise youthful effect.“You might get a longer lifespan but at the expense of something else,” Chang said. Instead, the researchers believe their work could point to a way of helping older people heal more quickly after surgery or boost organ function during illness. These short-term applications aren’t as likely to risk side effects that could accompany blocking such a critical protein. The work was supported by grants from the American Cancer Society, the National Institutes of Health, the National Cancer Institute and the California Breast Cancer Research Program. Other Stanford researchers who participated in the work are graduate student Tiara Kawahara and Jennifer Zhang, PhD, who was a postdoctoral scholar.

By Amy Adams