[extropy-chat] AGING: real progress

Joao Magalhaes 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  

More information about the extropy-chat mailing list