Current Research Into Telomeres III

Aubrey de Grey ag24 at mole.bio.cam.ac.uk
Thu Sep 3 08:59:56 EST 1998


Tom Matthews wrote:

> This is a reasonable way of looking at aging, IMO, except that we
> *know* that mitochondrial mutations and free radical damage (and AGE
> accumulation and many other things) *are* causal factors in normal
> aging, whereas we do *not* know that telomere shortening is.

to which William wrote:

> Well, I believe that there is more than enough evidence to prove that
> telomere shortening is a factor in human aging. What needs to be
> determined is whether telomere shortening starts causing problems
> after 100, 200, or 1000 years. 

I'm very pleased that emphasis is being laid on the difference between
showing that a phenomenon will eventually cause aging and showing that
it causes aging in a currently normal lifetime.  However, I'm afraid
we do not yet know for certain that mitochondrial mutations are causal
factors in normal aging (ie that they cause the macroscopic pathologies
which comprise aging).  We can say with confidence that free radical
damage (to proteins and lipids) and AGE accumulation are causal factors,
but we can't yet say what causes _them_ (to be precise, what causes their
accumulation to accelerate with age).  My own view is that mitochondrial
mutations are currently the prime suspect, but that's only because I see
a detailed mechanism whereby they _may_ cause these macroscopic symptoms,
and I don't see one for telomere shortening, dysdifferentiation etc.  The
only way we'll find out for sure is by actually demonstrating that such
a chain of events (perhaps the one I've proposed, perhaps another) really
occurs in the body.

Aubrey de Grey



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