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Current Research Into Telomeres III

Tom Matthews tmatth at netcom.ca
Wed Sep 2 20:14:30 EST 1998


ufotruth at ix.netcom.com wrote:
> 
> On Tue, 01 Sep 1998 21:23:54 -0700, Tom Matthews <tmatth at netcom.ca>
> wrote:
 
> >To be precise, are you saying that Rita Effros has found that the
> >*majority* of memory T-cells are now longer able to divide and produce
> >more such T-cells? Do you have a reference for this?
> 
> It would be pretty neat to read a reference for this.

But I could find any such.
 
> >Or since now you say "are approaching senescence" do you mean that she
> >found that the T-cells had reduced replicative ability in older people?
> >(which would not necessarily be related to any telomere shortening).
> 
> Well, they might not be related to any telomere shortening. That is
> very possible. There could be many things that cause this. But from
> what I have read it is at least "possible" that shortened telomeres,
> even not short enough to cause a cell to go into senecence, could
> cause a cell not to function as well as a cell with very long
> telomeres.

True, but there are many things which *could* be the cause of various
aging attributes! However, what we need to concentrate on right now is
what *is* the cause of even the most healthy people dying before age
120.

> >Certainly, because division "rate" is highly different in different
> >dividing systems and under different life, and health (sometimes
> >disease) conditions.
> 
> Interesting. Then perhaps by only restoring the telomeres in the cells
> that have had to divide many more times, because of somekind of stress
> or diesease, it could be beneficial to an entire organism.

Certainly, *if* cell senescence or even simply telomere shortening is
shown to be the cause of *some* aspect of aging decline, we could start
off with telomerase therapy for only those cells types, not *all*
dividing cells. 
 
>> Tahara H, et al, at Hiroshima University School of Medicine, Japan,
>> demonstrated that "a significant proportion of WRN, (Werner's syndrome), cell
>> strains showed drastic shortening or lengthening of telomere lengths during
>> cell passages compared with normal cell strains"  This confirms earlier
>> studies that Werner's syndrome and the childhood aging disease progeria
>> result from errors in the system(s) that maintain telomeric length.

> >But it doesn't say anthing about whether these diseases are related to
> >normal aging.
 
> Well, what is aging? In my opinion it seems to me that aging is just
> an accumilation of "diseases" in many different tissues. Whether they
> are from mitochondrial decline, telomere shortening, free radical
> damage, or anything else. So, if aging is caused by several different
> "diseases" then perhaps by eliminating all of the "diseases" we will
> eliminate aging.

This is a reasonable way of looking at aging, IMO, except that we *know*
that mitochondrial mutations and free radical damage (and AGE
accumulation and many other things) *are* causal factors in normal
aging, whereas we do *not* know that telomere shortening is.

> By stopping the worst of these diseases perhaps it would help an
> organism to live longer and healthier.

Again quite true, but neither progeria nor Werner's are diseases *of*
aging and neither may have anything to do with stopping normal aging.


--Tom 
Tom Matthews
 
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