On the surface it appears that the 14th theory of aging in my Anti-Aging Firewalls treatise Decline in Adult Stem Cell Differentiation is very different than the 12th theory Telomere Shortening. And these two theories seem to be different than the 2nd theory Cell DNA Mutation. However, a number of recent studies show a growing web of relationships among these theories. For example, telomeric dysfunction may be at the heart of the decreasing capability of stem and progenitor cells to replicate and renew tissues with increasing age (ref,ref,ref,ref). These and similar studies have looked at telomere shortening in hematopoietic stem cells (HSC), mesenchymal progenitor cells, osteoblasts and neural progenitor cells. One study suggests that proteins secreted from telomere-dysfunctional bone-marrow cells may provide accurate biomarkers of aging. As usual when it comes to aging, there are wheels within wheels. Among the many cellular proteins that influence telomere structure, function and enlongation are the telomerase binding factors TRF1 and TRF2 and less-directly shelterin-complex, PinX, Apollo and tankyrase(ref). TRF2seems to play a key role in the differentiation of neural stem cells(ref) as well as in cancer proliferation. In a closely related front, telomerase expression and TRF2 seem to play key roles in maintenance of DNA repair mechanisms in neural cells and stem cells(ref). While we are not there yet we are getting closer to a unified theory of aging. Also it is already clear how an anti-aging firewall intervention intended to address aging according to one theory, taking astragaloside IV as a supplement to activate telomerase expression, addresses aging according to several other of the theories as well.
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