It appears the prevailing theory as to why we age could be wrong–and that would be good news for anti-aging research (Via PhysOrg):
Age may not be rust after all. Specific genetic instructions drive aging in worms, report researchers at the Stanford University School of Medicine. Their discovery contradicts the prevailing theory that aging is a buildup of tissue damage akin to rust, and implies science might eventually halt or even reverse the ravages of age.
The “rust” the prevailing theory uses to explain aging is essentially the accumulated wear and tear caused by “toxins, free-radical molecules, DNA-damaging radiation, disease and stress.” But the results of the Stanford research, led by Stuart Kim, professor of developmental biology and of genetics, don’t fit that theory. Instead, they found that that hundreds of age-related genes in C. elegans nematode worms were switched on and off by a single transcription factor–a kind of signalling molecule–called elt-3, which becomes more abundant with age. Two other transcription factors that regulate elt-3 also changed with age. As a result, normal development becomes unbalanced in older organisms, something the researchers call “developmental drift.” And now that this mechanism has been found in one organism, scientists can look for it in others–including humans.
The idea that this developmental drift is behind aging rather than “rust” would explain why there are many animals that live far longer than humans:
Some tortoises lay eggs at the age of 100…There are whales that live to be 200, and clams that make it past 400. Those species use the same building blocks for their DNA, proteins and fats as humans, mice and nematode worms. The chemistry of the wear-and-tear process, including damage from oxygen free-radicals, should be the same in all cells, which makes it hard to explain why species have dramatically different life spans.
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If aging is not a cost of unavoidable chemistry but is instead driven by changes in regulatory genes, the aging process may not be inevitable. It is at least theoretically possible to slow down or stop developmental drift.
The research has been published in the July 24 issue of Cell; you can download the original paper in PDF format.
Having just celebrated another birthday and thus entered my 50th year on this planet, I can only say, “Faster, please!”
(Image: Wikimedia Commons.)
[tags]aging, biology, genetics, immortality[/tags]
I wouldn’t get too excited. This is not in any way contradictory of the `rust’ theory. Turtles are poikilothermic and wales hardly live in a similar environment to humans. I’m quite confident the accumulated genetic damage runs alongside. In fact, it may be the cause – apoptosis is a necessary part of growth and repair even in the embryo yet any problems with that process are, obviously, guaranteed to cause systemic failure.
Everything dies – whether it be worms or civilizations.
I recently passed that great meridian that separates the sea of the living from the sea of the dead myself. You have my sympathies. I suspect we’re going to be stuck with the very inferior ‘plan B’ – having to have our sorry bodies frozen (what’s left of ’em, anyway).