[ExI] reverse aging

Adrian Tymes atymes at gmail.com
Wed Dec 1 17:26:33 UTC 2010

On Wed, Dec 1, 2010 at 1:43 AM, The Avantguardian <
avantguardian2020 at yahoo.com> wrote:

> This means that if the telomeres are too short then the telomeric loop
> cannot form and the cell is *unable* to distinguish between the ends of its
> own
> chromosomes and a double-stranded break in its DNA. So it reponds to both
> the
> same way by shutting down the cell's ability to replicate itself. This
> is called
> cellular senescence.
> Cellular senescence is thought to contribute to aging by preventing the
> body
> from replacing cells when they die or wear out. But when a damaged cell
> manages
> to bypass cellular sensecence and tries to replicate itself despite being
> damaged, the cell will activate another program to try and commit cellular
> suicide called apoptosis. If apoptosis doesn't work, the cell is now a full
> blown turmor. So the cold hard truth about aging is that we are stuck
> between a
> rock and a hard place. In a certain sense, we get old in order to prevent
> cancer
> and if we get cancer, we don't survive long enough to get old.

What if you extended the telomeres, such that the only way senescence would
set in is via damage leading to cancer?  Maybe add in a very slow telomere
extending enzyme, that replaces telomeres fast enough for normal cell
division (to
replace worn out cells) but can't keep up - or even goes into reverse - if
very rapid
cell division is encountered (such as in cancer).  Might that work?
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