Since the discovery of these and other antiaging genes in lower organisms, the scientific search for live-longer genes in people has, not surprisingly, garnered much publicity. Often lost in the excitement about the prospect of triple-digit birthdays, however, is a far more realistic and immediate implication of the research. While learning how to extend the life span of humans could take many decades, if it's even possible, researchers are already using insights gained from studies of aging and the effects of calorie restriction to search for new drugs to treat the numerous diseases tied to getting old. The incidences of many illnesses, including cardiovascular disease, Alzheimer's, and cancer, rise nearly exponentially with age. And while we still don't know exactly why, we do know that calorie restriction -- at least in test animals -- delays the onset of a broad swath of these age-related diseases. "It's something people are surprised to hear, because it really begs the question, how is that possible? There must be some common metabolic component. But no one really knows how all those diseases can be tied together," says Guarente. Nevertheless, some biologists hope that a drug that mimics the molecular effects of calorie restriction might also delay the onset of some or all of these diseases. At least one company, Sirtris, a small but heavily funded startup in Cambridge, MA, believes it is close to finding such drugs. The company, which boasts an impressive group of prominent molecular biologists and geneticists on its scientific board, was cofounded by David Sinclair, a former postdoctoral researcher in Guarente's lab and now an associate professor at Harvard Medical School. Sirtris has come up with hundreds of molecules that activate the SIRT1 enzyme, which is produced by the mammalian homologue of sir2. (Seven different SIRT genes have been found in humans; these and their homologues in other species are collectively known as sirtuins.) If the company is on the right track -- and Sirtris says potential drug candidates for treating diabetes and neurodegenerative diseases are expected to begin preliminary human tests over the next several years -- the molecules could mimic the genetic effects of calorie restriction, offering its apparent health benefits without its drawbacks. "It's known that calorie restriction greatly enhances the body's natural ability to fight diseases," says Sinclair. The vital questions, he says, are what controls that process and whether we can develop drugs to target it. "We don't assume we know everything about it, but we do strongly believe that sirtuins are a major component in what could be a master regulatory system for human health." |
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How Cells Age
11/26/2008
Massachusetts Institute of Technology
Comments
Guest (Jeremy Villalobos) on 03/23/2006 at 12:00 AM
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voncanalchristie on 02/25/2007 at 5:22 PM
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Guest (James R Hughes, MD) on 04/06/2006 at 12:00 AM
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Guest (Steve Koelzer) on 04/10/2006 at 12:00 AM
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Guest (Steve Koelzer) on 04/10/2006 at 12:00 AM
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Guest (Bill Jackson) on 05/04/2006 at 12:00 AM
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One is the telomere length that is reduced bit by bit until the cell can no longer divide. Another is the gradual loss of the energy provisioning abilities of the mitochondria, which seem to act to limit cellular activity with advanced age.
If one transplanted some intact mitochondria from a long lived species into a short lived one, what would happen? Would the organism last longer? I suggest this be done first on related species with well known but short disparate lifetimes so the effect, if any, would be seen quickly.
Guest (Diane Ritter) on 08/03/2006 at 12:00 AM
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Guest (John Schloendorn) on 04/26/2006 at 12:00 AM
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I wonder how the author of this summary thinks a (presumably successful) treatment of age-related diseases can avoid resulting in life-extension... If we cure or postpone age-related diseases, i.e. things that kill us in old-age, then will we not almost by definition live longer?
rbarkley373 on 09/17/2007 at 2:36 AM
1