•With respect to the
accumulated damage theories (Oxidative damage, DNA damage, Mitochondrial damage, Incorrect protein folding ):
–Such damage will of course
occur; it occurs in younger as well as older people. The difference is that apoptosis and DNA repair mechanisms work much better in
younger people as is explained by the Programmed Epigenomic Changes theory. Also, dead cells in younger people are
replaced by ready stem cell
differentiation but not so in older people as explained by the Stem Cell
Supply Chain theory.
•With respect to
inflammation, immune system, susceptibility to cancer, cardiovascular and neurological disease theories
–There is widespread acknowledgement that
epigenomic reprogramming plays major roles in disease susceptibilities and development in these areas
–There is much current research on developing HDAC inhibitors as
preventative and therapeutic agents
for such diseases
–There is also much research
focusing on stem cell therapies in each of these disease areas and on aspects of operation of the stem cell supply chain
•With respect to the telomere
shortening theory of aging
–Expression of telomerase and
other factors affecting telomere length is determined by the epigenetic state of the cell
–It was once thought that
telomere shortening could be a major factor in the age-related decline of proliferative and differentiation capabilities of adult
stem cells. Lunyak’s work at the Buck
Institute suggests that the
smoking gun is instead damage to the RNA-encoded DNA damage repair machinery in adult stem cells.
•
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