In <4jjfbj$bsp at sydney1.world.net> GuyD at world.net (Guy Dunphy) writes:
>Then again, I'd be surprised if other age related problems (such as mechanical
>and structural wear and alteration) don't show up in the first experimental
>subjects to have their 'telomere aging' fixed.
>For instance, there's also the mitochondria functionality problem.
And the AGEs + other crosslinking problems, the free radical problems, the
lipofuscin and other garbage accumulation problems, the autoimmune problems,
the telomere-unrelated neoplasm problems, the protracted development
problems, atherosclerosis and other blood supply problems, a multitude of
homeostasis and "wear & tear" related problems, slow acting pathogens, and a
truckload of others. And let's not forget the progressive loss of cells
that can't divide in the first place.
Evolutionary theory predicts that there will be literally hundreds of
processes that contribute to what we call aging - and experimental observation
has done nothing but support such a prediction.
No observations that I'm aware of have shown telomere shortening to be a
significant factor in aging, and it's statistically unlikely that, with all these
other observed and predicted "aging" processes to compete with, it ever will.
>But I just have a gut feeling that telomere loss is the major cause of the
>'cellular death' clock. (Hope its not just wishful thinking.)
Maybe it is the major cause of cell death, but it remains to be seen just
what influence controlled "immortalised" cells would have on the aging of
an organism. Remember that your average 90-year-old human cell population still
has plenty of doubling potential in vitro, and we have no reason to assume that
it doesn't have even more in vivo (check out the effects of cortisol etc.) But you're
right, it would make for an interesting experiment.
Steve
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(I_lurk,_therefore_I_am!_\ ,,, Steve Chambers
(o o) steve at chambers.ak.planet.co.nz
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