[ExI] reverse aging

[Adrian Tymes]

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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