Cells and Aging
james at ryley.com
Wed Mar 3 23:59:51 EST 1999
Tom Matthews wrote:
> Thomas Mahoney wrote:
> > In article <36DB8C86.7A0A6342 at ryley.com>, james at ryley.com says...
> > >> It is my contention that "aging" is the result of the senescence or
> > apoptosis
> > >> of a significant number of cells in the system and that the "gradual"
> > >> approach to these states by individual cells does not play a large role in
> > >> the process.
> > >
> > >Aubrey might agree ;) I find it unlikely.
> > The evidence that cellular loss or thinning of cell walls is conducive to
> > artheriosclerosis, that the majority of cancerous cells have by-passed
> > senescence and that much immunological deterioration is the result of T-cell
> > senescence all suggest that it is late stage cellular development or lack
> > thereof that contributes the most to systems failures.
> IMO, all three of those premises go far beyond what is proven.
> 1. There is no proof that any thinning of cell walls (I assume you mean
> arterial walls here) even if conducive to artheriosclerosis is caused by
> apoptosis generated by a reduction of telomere length of any cells.
> 2. The majority of cancer cells have bypassed senescence because all the
> ones that did not are not detected because they have not caused the
> symptoms of cancer. Furthermore, this likely has little relevance to
> aging since the DNA in those cancer cells was mutated in such a way as
> to make them divided more often than others of their kind or again they
> would not have gotten to where they needed to by-pass senescence.
> 3. Finally, there is only evidence that T-cell senescence *may* be the
> cause of immune deterioration in *some* cases (perhaps even likely in
> AIDS). To conclude that T-cell senescence many be the cause of *all* or
> even *most* immunological deterioration goes far beyond reason.
> Since every one of your premises are so unproven, your conclusion that
> "it is late stage cellular development or lack thereof that contributes
> the most to systems failures" is wild conjecture in the extreme based on
> current available evidence.
> Tom Matthews
I'd like to add one point ot this discussion: Being more generous
than Tom Matthews, I will allow that Tom (Mahoney) could be right
-- FOR THE EXAMPLES THAT HE PICKS. But, he is making broad
generalizations that are inappropriate even if he had the
evidence to support his specific examples.
You just can't say "This is what we see in T-cells (or
fibroblasts, or anything), so this is how aging works." We have
over 200 different cell types in our bodies. They all have
different metabolisms, evolved for different purposes, and are
subject to different stresses. There is no reason to hypothesize
that they all experience aging in the same fashion.
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