Proliferative Theory of Rejuvenation

Jurgen Kaljuvee kaljuvee at HUSC.HARVARD.EDU
Thu Jan 23 02:04:55 EST 1997

As I understood it, the main idea of Fossel's book 'Reversing Human Aging' 
was that ensuring near-infinite cell division will constitute a 
repair mechanism for cytoplasmic cellular damage. But how good is this
mechanism? That is, can reactivating telomerase and bestowing somatic
cells with near-infinite proliferative capacity ensure arresting or even
reversing aging, as Fossel claims? True, cells that are particularly
heavily damaged will be programmed to apoptosis and replaced by adjacent
cells but how will the adjacent cells escape cumulative damage, in both
DNA and cytoplasm (isomerization, free radicals etc)? Where is this source
of undamaged cells?  It seems that for Fossels theory to work we need a
source of cells with fresh undamaged DNA but there is no such source
unless we design additional, artificial repair mechanisms for the cell.

To paraphrase, it seems that it would be difficult to escape the 'normal'
pathology (i.e., pathology NOT associated with telomere shortening)
and it seems that ensuring the proliferation of cells by reactivating
telomerase will extend the lifespan BUT UNDER NO CIRCUMSTANCES STOP AGING
OR REVERSE IT (as the title of the book suggests).  Thus, using the
language of mathematicians, ensuring infinite proliferative capacity is a
necessary but not a sufficient condition for arresting aging (because
telomere shortening is only one of many causes of aging).  

So the best we can do in the near future is to get rid of the component of
aging associated with telomeres and that should increase the life span a
little.  I think we cannot yet say by how much, though Fossel predicted
400-500 years (how?). The only experimental evidence for
this that I know of (Shay, Wright paper in EMBO) was, though pioneering,
not really therapeutic. Is there new evidence out there?

I would be happy to hear any comments.

Jurgen Kaljuvee

kaljuvee at fas.harvard.edu

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