Scientists have already reversed the aging process in mice that they had engineered to age prematurely.
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Telomere Tweaks Reverse Aging in Mice
By Brandon Keim November 29, 2010
wired.com
By tweaking enzymes that prevent chromosome tips from unraveling, researchers have shown age-related tissue degeneration can be reversed in some mice.
Medical breakthroughs involving mice must be taken with rock-sized grains of salt because, despite their superficial genetic similarity, rodents are a very long way from humans. The latest findings, published online by the journal Nature on November 28, are no exception. Nevertheless, they provide the first compelling evidence of aging’s reversal — not just delay — in a high-level organism.
The work represents an “unprecedented reversal of age-related decline in the central nervous system and other organs vital to adult mammalian health,” wrote the team led by Ronald DePinho, a cancer geneticist at Harvard Medical School.
The researchers genetically engineered mice to lack telomerase, the key enzyme ingredient in structures called telomeres that cap the tips of chromosomes and prevent them from fraying. In healthy mammals, telomeres shorten slightly with each round of cell division and such shortening is linked to a variety of age-related disorders.
DePinho’s telomerase-less mice tended to be prematurely aged and infertile with small brains, damaged intestines and poor senses of smell. Four weeks after the researchers gave them a drug designed to stimulate telomerase production, however, these visible signs of aging had reversed.
In a press release, DePinho described the transformation as “akin to a Ponce de León effect,” referring to the 16th century conquistador’s search for a fountain of youth.
It may be a premature choice of phrase. Before speculation on human applications can even begin, the researchers need to determine whether telomerase activation works for “normal” mice, and not just a single strain genetically engineered to age prematurely.
Such strain-dependent effects have confounded the promise of drugs designed to mimic the apparent longevity-extending effects of low-calorie diets. But even if the findings are never translated directly to humans, they may still provide insight into the physiological basis of aging itself — something that, despite centuries of study, has yet to be pinned down. |
