Interesting that telomeres appear to play no role in either human skin aging, or bone marrow aging.
Aged skin was associated with thinning of the epidermis, decreased proliferation, and increased apoptosis below the granular layer. This was associated with increased epidermal expression of Fas and FasL. Telomerase activity was similar in aged and young epidermis. CONCLUSIONS: Fas/FasL-mediated apoptosis, along with decreased proliferation, may have a role in changes of human epidermis during ageing. Telomerase activity did not appear to be limiting in young vs. old human epidermis.
It is quite surprising that some major manifestations of aging such as skin and muscle atrophy can be reversed in old animals (or induced in young animals) by transplantion and/or joining of blood streams (parabiosis). It would be interesting to know how many signs of aging are due to immunological and systemic factors rather than tissue specific factors like telomeres.
We know that telomeres generally become shorter with age. We also know that errors in telomere mechanisms - much more common for shortened telomeres - are a root cause of many cancers. We know that telomere malfunctions are implicated in Werner's syndrome, an accelerated aging condition. Beyond this, the story seems to get much more complex - stay tuned.
You might want to read up on recent insights into the way in which the immune system deteriorates with age - scientists are closing in on the precise mechanisms by which this happens. This is a very promising sign for the prospects of future rejuvenative therapies for the immune system.