Ageing/AIDS similarity:
On 10 Apr 1996, Mike West wrote:
> Mail*Link( SMTP FWD>RE>Premature Ageing
>> There actually is quite a bit of evidence of a causal connection between
> telomere loss and cell aging and also cell aging and organismal aging. In
> regard to the former, or course, telomeres are lost in mortal cells that lack
> telomerase, immortal cells like the reproductive cells, have abundant
> telomerase and stable telomeres and when cells immortalize as in cancer they
> abnormally acquire telomerase acitivity. This is correlative evidence.
> Recently, U.T. Southwestern published in EMBO J evidence of causality,
> extending the telomereres of cells increased their replicative capacity as you
> would predict.
>> In regard to evidence that cell senescence is occuring in vivo, the evidence
> is seen in many ways. Cells cultured in primary cultures from old people's
> tissues contain many large nondividing cells that have many markers of cell
> senescence (morphological, gene tag markers, enzyme markers such as beta gal,
> and lastly telomere length) For instance in the case of skin, dermal
> fibroblasts from aged donors turn blue in X-gal as do cells at the Hayflick
> limit and telomere length has been shown to shorten in the skin with age.
> When the beta-gal assay was performed on skin sections in situ, blue cells
> were shown to be present only in donors over the age of 30 or so, and only a
> percentage (probably less that 50%) were seen to show senescent markers even
> in very old donors. But this is what many would expect, that is, that cell
> senescence in a minority of cells can have a dominant effect on tissue
> metabolism.
>> Personally, I like to say that no one dies of old age, but rather, we die
> because of disease.
This sounds like AIDS. Curing AIDS and AGE have common objectives.
AIDS gets more publicity and support from the media, however, as well as
from the general public. Why is that? Why is there so much more hype
about AIDS than AGE? AIDS just works a few years quicker.
Those interested in AGE research may consider the political and promotional
strategies of the proponents of AIDS research. Alert the media. Alarm
the public. Light a fire.
> But that isn't to say that disease and aging aren't
> sometimes the same thing. If we defined age-related pathology not as the many
> pathologies that simply increase in frequency with age, but as pathologies
> that virtually everone sees manifestations of in advanced age (such as
> atherosclerosis, AMD, osteoporosis, etc, then maybe, these pathologies are
> actually the manifestation of aging in that given tissue (i.e. sometimes a
> senescent cell may be a "sick" cell.
>> --------------------------------------
> Date: 4/1/96 2:46 PM
> From: jpissa at welchlink.welch.jhu.edu> Oliver Bogler <obogler at ucsd.edu> wrote:
>>> >This is all very interesting, but you seem to unaware that there is no
> evidence of a
> >connection between telomere length/cellular ageing and organismal ageing.
> Organismal
> >ageing is better discussed in terms of mortality - no one dies of "old age".
> There is
> >always a "pathology", and that has nothing to do with telomere length.
>>> You are right to point out the shortcomings of the current 'Telomere'
> theory of aging. Nevertheless, it is not entirely clear that no one
> dies of 'old age'. Autopsy studies indicate that 20-30% of deaths in
> the elderly cannot be attributed to a specific pathology. While this
> may certainly be due to missed diagnoses, this proportion of 'unclear'
> cause of death is higher than that seen in autopsy studies of younger
> individuals. I think that the notion of dying of 'old age' i.e.
> because of a limited lifespan that is not disease related remains open
> for discussion. Any comments anyone ?
>> Jean-Pierre Issa MD
> Johns Hopkins Oncology Center
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> To: ageing at net.bio.net> From: jpissa at welchlink.welch.jhu.edu (Jean-Pierre Issa)
> Subject: Re: Premature Ageing
> Date: Tue, 02 Apr 1996 00:49:28 GMT
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>>>>>
