“It’s a fundamental finding,” says Huber Warner, associate dean for research at the University of Minnesota, in St. Paul, and editor of the Journal of Gerontology. But it’s far from clear if this drift is also at work in people, he says. “The most important conclusion from this paper is that the basic mechanism of aging in these two kinds of species is fundamentally different,” says Warner. “If it does apply to mammals, it’s not as important as it is in nematodes.”
Mammals may be more susceptible to accumulated wear and tear, he says, because cells are continually damaged and replaced from a pool of stem cells present in most tissues. Too much stress destroys the ability of stem-cell pools to replace tissue. Worms, on the other hand, are generally stuck with the cells that they’ve got once they hit adulthood: most cells are no longer capable of proliferating.
Kim’s team is now studying the human versions of these genes. While it’s unlikely that the same genes are involved in human aging, he says, “I think that the conceptual idea that known human-developmental controls are not maintained as people grow older is attractive and theoretically possible.” However, “there is no direct evidence for developmental drift in mammals yet,” he says.
If developmental drift does turn out to play a role in human aging, it could be good news for drug developers. Scientists are currently trying to mimic the effects of some life-extending interventions–most notably, caloric restriction (a diet low in total calories but with adequate nutrition)–with drugs. But when it comes to longevity and the diseases of aging, new drug targets are always welcome.