Re-Visiting a Post by Lou Pagnucco
ufotruth at ix.netcom.com
ufotruth at ix.netcom.com
Fri Oct 23 15:30:05 EST 1998
>Senescent cells appear to accumulate in tissues with age. Furthermore at
>least some of these cells, like fibroblasts, can be identified by their
>profile of enzymatic activity and stained so that they are clearly visible
>under the microscope.
Absolutely correct. But also old cells, which are not yet senecent,
also accumilate in tissues.
>( See the description of Judith Capisi's work at the
>Now, senescent fibroblast produce many times the amount of collagenases
>- possibly the most important family of enzymes responsible for the
>degradation of the extracellular matrix. Are these senescent fibroblasts
>responsible for some of the features of aging like lax skin, overly permeable
>capillaries, breakdown of the blood-brain-barrier, some arthritic conditions,
Most probably the accumilation of senecent cells, and older cells that
are nearing senecence, both contribute to many of the symptoms of
>If so, since they can be identified by staining, can they also be targeted
>by smart drugs which have special affinity for these cells and selectively
>toxic to them? directly toxic, phototoxic, or apotosis inducing ?
The problem would be that by eliminating the senecent cells it would
cause the other cells to divide and replace them. This would cause
more telomeres to be lost that would cause more senecent cells and old
cells to accumilate.
But it might work very well IF all of the non-senecent or old cells
are immortalized with the telomerase gene. That way when they divided
to replace the senecent and old cells they would not cause an
accumilation of senecent and/or older cells.
>I'm reposting a post of yours from a while back. At that time I indicated
>that I didn't think this approach would be beneficial since the remaining
>cells would reproduce and just generate more senescent cells.
Personally, even though I might be wrong, I still don't think that
approach would be beneficial. At least not in the long term.
>After reviewing the research of Dr. Effros at U.C.L.A. in regards to
>immunosenescence it appears that the strategy you suggested may be of some
That is possible. But anything that causes cells to divide will
shorten telomeres and eventually cause an accumilation of senecent and
>From Dr. Effros work including, (Am J Hum Genet 1998 May;62(5):1003-7
>"Replicative senescence in the immune system: impact of the Hayflick limit on
>T-cell function in the elderly."), it appears that one of the negative
>effects of senescent cells, at least in T-cells, is that they inhibit the
>production of more functional cells. Elimination of these senescent cells
>may allow for the production of other more productive cells.
But having the more productive cells divide to replace the senecent
cells would only cause an increased rate of cellular aging. It may
temporarily allow for more productive cells to be in tissues but it
would also cause an accelerated rate of aging, unless you immortalized
the healthy, productive cells first.
>Additionally, even if the remaining cells did progress more rapidly toward
>senescence, due to this increased cellular production, the majority of them
>would initiate apoptosis rather than becoming senescent. Thus the overall
>effect may very well be improved functioning of the system(s) in which this
>strategy of eliminating senescent cells were employed.
But before they reach senecence, or initiate apoptosis, they would
still divide more times, age, and cause many problems.
Just because an older cell is not "senecent" does not mean it is a
healthy cell and just as functional as a "young" cell.
Thanks for your very interesting and informative post Thomas.
Take care and have a great day.
>Thomas Mahoney, Pres.
>Lifeline Laboratories, Inc.
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