From: Joao Magalhaes (jpnitya@skynet.be)
Date: Tue Jul 23 2002 - 14:33:28 MDT
Hi!
I haven't read Van Zant's latest paper but I read some of his earlier work
and his ideas make sense. The first paper on aging that I published was
called "Fighting aging at its core" and it argued that the best places to
find the causes of aging are the core regulatory pathways. For example, the
DNA is an intuitive candidate since it's where the "program" is located.
Now, if stem cells play the critical role so many argue then having DNA
damage in stem cells as a cause of aging is quite intuitive. Unfortunately,
as in so many other theories of aging, this reasoning fails to answer some
key questions: How do we know that stem cells aren't in turn controlled by
something else? (For example, brain signals, as Tuck Finch argues.) Why do
humans age so slower than mice? Why do bats age so slower than mice? (Bats
and mice have roughly the same size and the same metabolic rates.) Anyway,
it's an interesting hypothesis and I'll be checking the genes you mention
in Medline.
At 12:04 23-07-2002 -0700, Robert wrote:
>The Rad50 possibility is quite interesting because it fits
>in well with my see-saw theory of aging vs. cancer in
>choosing the Non-homologus end-joining vs. homologous
>repair pathway for DNA double strand breaks. Choose
>NHEJ and the genome gradually becomes corrupted and
>you get aging. Choose HR and recessive alleles that
>were masked begin their ugly heads.
Lately, I've been moving toward the DNA damage theory. Yet I'm not sure as
to how it can work. I mean, somatic mutations don't appear to be the cause
of aging -- take Dolly as a proof. One hypothesis I've been thinking is
that aging alters the chromatin structures and thus affects gene expression
-- there are some results from yeast that show gene silencing due to
different structures of the chromosomes. Telomeres also affect gene
silencing and the chromatin structures.
As for your theory Robert, if I understand it correctly, you're talking
about a typical accumulation of somatic mutations due to NHEJ. So, how do
you explain Dolly and all the clones?
All the best.
Joao Magalhaes (joao.magalhaes@fundp.ac.be)
Website on Aging: http://www.senescence.info
Reason's Triumph: http://www.jpreason.com
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