[extropy-chat] AGING: real progress

[Joao Magalhaes]

Hi!

I don't want to be the skeptic around here but I should remind you that 
there is NO evidence SIRT1 is in anyway involved in human aging. Yes, in 
yeast sir2 is involved in cell cycle regulation--which is not the same as 
aging. Maybe sir2 is involved in aging of C. elegans but results from 
Drosophila and mice do not suggest any involvement of SIRT1 in aging. Since 
drosophila and mice are biologically closer to humans than c. elegans and 
yeast, I'm skeptical that SIRT1 plays a role in human aging.

As for the Forkhead family, these transcription factors are very much 
involved in development, so it is normal that they affect redox potential 
and apoptosis. Nevertheless, I wouldn't be surprised if they were involved 
in mammalian aging since p66 has been associated with the forkhead family. 
Yet the connection to human aging is not clear because of cancer. After 
all, yeast, drosophila and c. elegans don't have cancer and mice have much 
higher cancer incidences. So we must be very careful in extrapolating this 
sort of data into humans.

-- End of skeptical message --

Joao

At 10:22 21-02-2004 -0800, you wrote:

>Well, we finally have some real progress on understanding aging.
>
>It looks like SIRT1 (homologue of yeast Sir2), regulates FOXO3
>which in turn regulates the enzymes that resist oxidative stress.
>
>Science Daily:
>http://www.sciencedaily.com/releases/2004/02/040220081158.htm
>PubMed Abstract:
>http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14976264&dopt=Abstract
>
>Now *before* everyone gets all excited please note that the
>gene regulation goes against apoptosis (programmed cell death)
>and for stress resistance (particularly from free radicals).
>That is probably a reasonable strategy in short lived animals
>(which include most that scientists work on in labs).
>
>However in long lived larger organisms one does not want to suppress
>apoptosis (because it will probably lead to an increase in cancer).
>In long lived species one needs to allow apoptosis or improve the
>ability of the immune system to recognize and eliminate cancer cells
>(which people are working on).  One also needs to promote stem cell
>replacement of lost cells (which we have some of but it probably isn't
>as finely tuned as one would like).
>
>But it is clear that this provides a key piece of the puzzle as
>to how cells manage the repair/replicate/die decision processes.
>Now whether the actions of FOXO3 on apoptosis and stress resistance
>have been split in longer lived organisms (so one has 2 genetic
>programs under individual controls rather than just a combined
>genetic program with only 1 control factor) remains to be seen.
>
>Robert
>
>
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Joao Magalhaes (joao.magalhaes at fundp.ac.be)

Website on Aging: http://www.senescence.info
Reason's Triumph: http://www.jpreason.com