Re-Visiting a Post by Lou Pagnucco
Aubrey de Grey
ag24 at mole.bio.cam.ac.uk
Fri Oct 23 13:54:41 EST 1998
> But I don't think lax skin has much to do with collagen
> crosslinking (other than some decreased elasticity). I think
> loss of subcutaneous fat is the culprit
I don't quite understand this. Loss of subcutaneous fat will cause
lax skin only if the skin can't contract to take up the slack; the
decreased elasticity is what removes this capability, no? So they
are both culprits, but reversal of either would be a remedy.
> > It seems relatively feasible to use either the increased production
> > of collagenase or that of beta-galactosidase for this purpose.
> That seems a lot harder to me than you seem to think. That would
> mean that you need to come up with a toxin that is activated by
> the enzymatic activities of one of these enzymes.
Or by its simple presence.
> It would be a lot easier ... to create an
> immunotoxin to a cell surface feature that only senescent cells
> have (or that they have a lot more of).
Sure, but the feature need not necessarily be on the surface -- a toxin
that enters all cells and is activated only by a very high intracellular
concentration of the feature would be enough. We are thus not restricted
to molecules that are bound to the cell surface. Of course the target
that proves best is also rather likely to vary from one cell type to
the next, so it may be profitable to keep such options in mind even if
their technical details are a little more intricate.
Aubrey de Grey
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