In article <3lmk3b$o03 at news.halcyon.com>, venezia at zgi.com (Domenick
Venezia) wrote:
> Is senescence not a probabilistic process with a presumably gaussian
> distribution? Don't we lose individual stem cells one at a time? The
> stem cells left in a 120 year old are simply those few on the extreme
> right of the distribution. Couldn't this be the reason our skins get
> thinner, and our digestion gets poorer as we age? The number of stem
> cells regenerating these tissues is less, and the tissue regeneration is no
> longer as robust? So I think the Hayflick limit is active in human stem
> cells, and isn't that the whole implicit assumption of the
> telomere/telomerase work? That shortened telomeres lead to senescence
> of stem cells and that the result of that senescence is the Hayflick
> limit? If you have data that suggests that human stem cells in vivo are
> in fact immortal I'd like to have a look at it, because it would completely
> change the way myself and many others think about aging.
Cellular senescence does not appear to be probalistic in the sense that a
cell has a given probability of senescing per division. In fact whole
populations of cells senesce near-simultaneously in some model systems
(eg. rodent embryo fibroblasts) which has led to the suggestion that a
cellular clock regulates the onset of senescence. This is the main line of
work that supports the view that cellular senescence, and so possibly
organismal ageing, is an active process rather than the random
accumulation of damage.
The telomere hypothesis is one possible mechanism by which the postulated
cellular clock could operate. At the moment the data are only correlative:
telomere length/telomerase activity and expecte cellular lifespan
correlate. But I need hardly say that that is not proof of causation.
As to data that says that human stem cells *in vivo* are immortal - a bit
hard to come by? Once we know what the basis of the Hayflick limit is, we
could more easily go look.
Oliver
