[extropy-chat] AGING: real progress
jpnitya at sapo.pt
Sun Feb 22 23:15:34 UTC 2004
I agree with the argument that the essence of life is very similar amongst
eukaryotes. I mean, the way the system is designed is similar between yeast
and human cells. Yet unicellular organisms don't need apoptosis and thus
linking findings in yeast sir2 to findings in human cells with SIRT1 and
apoptosis is dubious.
As for p66, the main interest in it is that knocking out p66 in mice
increases their lifespan and may also delay aging. Since p66 is related to
apoptosis, and mice have tons of apoptosis, my opinion is that p66 -/- mice
live longer because of changes in tissue homeostatsis caused by having
lower levels of apoptosis. I very much enjoyed the ideas in:
Warner, H. R., and Sierra, F. (2003). "Models of accelerated ageing can be
informative about the molecular mechanisms of ageing and/or age-related
pathology." Mech Ageing Dev 124(5):581-587.
Although Warner mentions his ideas in the context of models of accelerated
aging, I tend to see the delayed aging witnessed in p66 mice as similar.
You can also easily extrapolate these models into Werner's syndrome.
All the best,
Joao Magalhaes (joao.magalhaes at fundp.ac.be)
Website on Aging: http://www.senescence.info
Reason's Triumph: http://www.jpreason.com
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