aging

Investigators rejuvenate stem cells in aging study

John Carroll — Mon, 16 Jun 2008 19:24:23 -0400

Research at UC Berkeley is pointing the way to new therapies that can blunt or even reverse the effects of aging on muscles. In a new study led by Irina Conboy, a team of scientists determined that a molecule called TGF-beta played a key role in the deterioration of muscles. Blocking that pathway in mice reversed the physical effect in older mice. The researchers used RNAi technology to silence the molecule and then used snake venom to damage their muscles in the experiment. Older mice were able to produce new stem cells to repair the muscles, much the way that young mice were able to.

"We are one step closer to having a point of intervention where we can rejuvenate the body's own stem cells so we don't have to suffer from some of the debilitating diseases associated with aging," said the study's lead author, Morgan Carlson, a recent Ph.D. graduate of Conboy's lab.

- read the report from MIT Technology Review

Buck Institute to tackle aging research with stem cell funds

John Carroll — Tue, 03 Jun 2008 08:45:23 -0400

The Buck Institute for Age Research was the only non-academic group to receive California stem cell grants for new research facilities this year. After qualifying for $20.5 million in state funds, the institute now plans to build a 65,000-square-foot research center on its campus in Novato, CA. When the $41 million facility opens, the institute plans to expand its work in the field of aging and chronic diseases as researchers explore ways to expand the average life span beyond its current limits.

"We think the link between aging and getting diseases has really been under-appreciated," James Kovach, the Buck Institute's president and COO, told BioRegion News. "It's really looking at healthy populations earlier, and then understanding the aging process so that you can delay it. By delaying the aging process, we believe you'll delay the onset of virtually every chronic disease in parallel. We refer to it as the longevity dividend [that results] if you can help people avoid chronic diseases, particularly in the 60s and 70s, so that essentially people live a healthy life--the clinical reference to that is compressing morbidity."

- check out the release on the funding
- read the Q&A from BioRegion News

Longevity gene may be key to living past 100

Tue, 28 Aug 2007 06:59:59 -0400

Studying a group of Ashkenazi Jews noted for their long lives, scientists at the Albert Einstein College of Medicine say that longevity genes appear to be responsible for fighting off disease-causing genes in the very old, a condition that causes more disease-causing genes to build up over a person's lifetime. The researchers speculate that it may be possible that a single longevity gene buffers against disease-causing genes, which would open the way to developing new therapies that would mimic the activity of that gene. The Einstein researchers are expanding their longevity research, using high-throughput technology to go beyond the 66 genetic markers involved in this study. They're looking for genetic networks that play a role in aging.

"This study shows that our approach, which was inspired by a theoretical model, can reveal underlying mechanisms that explain seemingly paradoxical observations in a complex trait such as aging," says Dr. Aviv Bergman. "So we're hopeful that this method could also help uncover the mechanisms-the gene interactions-responsible for other complex biological traits such as cancer and diabetes."

- check out the release on their work

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Press Release: Reducing Insulin Signaling in the Brain Can Prolong Lifespan

Maureen Martino — Tue, 24 Jul 2007 11:45:38 -0400

One route to a long and healthy life may be establishing the right balance in insulin signaling between the brain and the rest of the body, according to new research from Children’s Hospital Boston. The study, published in the July 20 issue of Science, not only reinforces the value of exercising and eating in moderation, but also helps explain a paradox in longevity research.

Insulin sends a vital signal throughout the body telling cells to use sugar from the blood. But when cells become less sensitive to insulin, which often happens as we age and gain weight, the body must make more insulin to keep sugar under control and avoid type 2 diabetes. For a long time, clinicians and scientists thought that “more insulin was a good thing,” says Morris White, PhD, a Howard Hughes Medical Institute investigator in Children’s Division of Endocrinology, who led the new study. “But the increased insulin also gets into the brain, where it can be detrimental.”

Studies in the worm C. elegans and in fruit flies show that reducing insulin signaling lengthens lifespan. But in humans and rodents, reducing insulin signaling often causes diabetes. The view that insulin could reduce lifespan is difficult to reconcile with decades of clinical practice and scientific investigation to treat diabetes.

White suspected that the key to explaining this paradox—and to maximizing both health and longevity—is to reduce insulin signaling only in the brain. To test this idea, White’s team measured longevity and other characteristics in several groups of mice. In one group, they used a genetic trick to cut in half the amount of Irs2, a protein that carries the insulin signal inside the cell, in every cell of the body. Two other groups of mice were genetically engineered to have half, or nearly all, Irs2 removed only from the brain cells. Another group of normal mice served as controls.

“To our surprise, all of the engineered mice lived longer,” says Akiko Taguchi, PhD, first author of the study. Even more surprising, the mice lacking Irs2 only in the brain lived almost half a year longer than the normal mice – an 18 percent increase in lifespan – despite being overweight and having higher blood insulin levels, changes that usually reduce lifespan. These long-lived mice were more active in old age, retained youthful metabolic cycles (burning sugar by day and fat by night) and retained protective levels of anti-oxidant enzymes such as superoxide dismutase, which protect against oxidative stress, or “biological rusting,” in the brain and body.

The mice with normal brain Irs2 levels aged less gracefully – they lost the metabolic rhythms of youth, became more sedentary, and had reduced anti-oxidant enzymes after meals, leaving them vulnerable to cellular damage. Such damage correlates with a host of age-related diseases such as atherosclerosis, Alzheimer’s disease and cancer, notes White.

White believes the study findings suggest a new approach to preventing diseases that shorten lifespan. “The engineered mice live longer because the diseases that kill them – cancer, cardiovascular disease and others – are being postponed by reducing insulin-like signaling in the brain,” he says, “regardless of how much insulin there is in the rest of the body.”

Drugs that regulate Irs2 signaling in the brain (but not elsewhere in the body) are one possible preventive strategy, but no such drug has yet been found. Targeted drugs will be important because Irs2 is needed in other tissues, particularly the pancreatic beta cells that produce insulin.

“The easiest way to keep insulin levels low in the brain,” White says, “is old-fashioned diet and exercise.” Although obesity and sedentary lifestyles tune down the body’s sensitivity to insulin, exercise can bring it back and reduce blood insulin levels. Eating smaller meals keeps insulin low in the bloodstream, ensuring that less reaches the brain. The new drugs designed to fight insulin resistance and type 2 diabetes might have a similar effect.

“This study provides a new explanation of why it’s good to exercise and not eat too much,” says White. “It has less to do with how we look, and more to do with a healthy brain, especially in old age.”

The study also calls into question the long-term effects of insulin therapy for diabetes, White adds. “High insulin should be the short term solution to insulin resistance, because it might damage the brain in the long run,” he says. Better treatments for diabetes and healthy aging, he suggests, should concentrate on sensitizing the body’s cells to low amounts of insulin.

The work was supported by the Howard Hughes Medical Institute, the National Institutes of Health, the Japan Society for the Promotion of Science and the Yamada Science Foundation.

Children’s Hospital Boston is home to the world’s largest research enterprise based at a pediatric medical center, where its discoveries have benefited both children and adults since 1869. More than 500 scientists, including eight members of the National Academy of Sciences, 11 members of the Institute of Medicine and 10 members of the Howard Hughes Medical Institute comprise Children’s research community. Founded as a 20-bed hospital for children, Children’s Hospital Boston today is a 347-bed comprehensive center for pediatric and adolescent health care grounded in the values of excellence in patient care and sensitivity to the complex needs and diversity of children and families. Children’s also is the primary pediatric teaching affiliate of Harvard Medical School.