From: Robert J. Bradbury (bradbury@www.aeiveos.com)
Date: Tue Oct 05 1999 - 03:32:51 MDT
I'm not going to quote the comments, but simply add my
two cents worth to this discussion.
I *really really* wish people would get off the whole telomere kick.
Telomeres and telomerase are to a large degree irrelevant to the
longevity of your *mind* unless you intend to stay in your current
biological body indefinately.
Telomeres are *only* important for dividing cells, that means
your epithelial cells or "external" cells that are exposed
to environmental wear and tear in some way (skin, gut, lung)
and perhaps the endotheilial cells (on the surfaces of your blood
vessels). They may also play a role in which hyperactive cell division
occurs such as cancer or AIDS.
Fossel did the aging field a huge disservice when he suggested
that telomeres explain relatively all aspects of aging. Brain
aging is much more likely to be based on mitochondrial DNA
damage leading to energy insufficiency and/or cell death and/or
recombination and shortening in the repeated ribosomal DNA sequences
leading to a reduction in protein synthesis. Neurons do not divide
and so telomere shortening is unlikely to be involved in
their "aging" (Fossel's suppositions that they effect
glial cells and indirectly neurons is a real stretch).
So with regard to clones & telomeres the only question becomes
what impact does shortened telomeres have on "cloned" organisms?
In short it makes them less healthy and causes some organ systems
to age more quickly. If you create an organism with shorter
telomeres than the natural version, then those tissues that
depend on dividing cells are likely wear out more quickly.
Is this significant? Not if we plan to replace those organ
systems with versions grown in pigs or laboratory grown
equivalents. Also irrelevant if we plan to upload.
Also *completely* irrelevant if you envision being able
to augment the genome with multiple genes with a ten
year time frame or completely replace the genome with
an alternate program within a 20 year time frame.
The telomere shortening appears to only affect genes on the
ends of 2-6 chromosomes (see work by Olivia Pierra-Smith),
so whatever is involved as effectors downstream from the telomeres
can be replaced, adjusted, augmented, etc.) with complete disregard
to the telomere length once we undertand the location and function
of those genes.
So please, if you want to drag up telomeres or telomerase, drag
them up with a disclaimers about *what* specifically you want to
apply them to that has real significance to our evolution and
long term survival. From my perspective they represent a
lot of noise that actually distracts us from the real problems
in aging and longevity.
Robert
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