Numerous studies now show that stem cell populations in old tissues remain large, and have explored a few of the mechanisms that explain why these stem cells are no longer as active in tissue maintenance as they were in youth. In a number of cases researchers have been able to demonstrate partial reversal of this decline by altering the signaling environment, overriding the age-related changes that seem to be responsible without addressing the underling causes of these changes, which are no doubt reactions to rising levels of cellular damage.
It is likely that researchers will find naive applications of this sort of restoration of stem cell activity will greatly raise cancer risk, as cancer suppression is probably the reason why stem cells have evolved this diminished action response to the damage of aging - our longevity is thought by many researchers to be a balancing act between risk of cancer and levels of tissue maintenance in an environment of steadily rising damage. The ability to detect and selectively and safely treat cancer is improving rapidly, however, so a blunt restoration of stem cell activity may well turn out to be an acceptable stop-gap approach to improve health in old age:
Previous studies have demonstrated an age related decline in the size of the neural stem cell (NSC) pool and a decrease in neural progenitor cell proliferation, however, the mechanisms underlying these changes are unclear. In contrast to previous reports, we report that the numbers of NSCs is unchanged in the old age subependyma and the apparent loss is because of reduced proliferative potential in the aged stem cell niche.
Transplantation studies reveal that the proliferation kinetics and migratory behavior of neural precursor cells are dependent on the age of the host animal and independent of the age of the donor cells suggesting that young and old age neural precursors are not intrinsically different. Factors from the young stem cell niche rescue the numbers of NSC colonies derived from old age subependyma and enhance progenitor cell proliferation in vivo in old age mice. Finally, we report a loss of Wnt signaling in the old age stem cell niche that underlies the lack of expansion of the NSC pool after stroke.