Telomeres and Aging (links) Many scientists previously thought that aging might arise primarily due to clock-like shortening of telomeres, DNA-protein complexes at the end of each of our chromosomes, with every cell division. This was primarily based upon in vitro experiments wherein the lifespan of cell cultures could be extended past the Hayflick limit (roughly 50 cell divisions) via the addition of telomerase, an enzyme that elongates telomeres. They postulated that telomeres served to prevent cancer cells from dividing indefinitely by cutting off their proliferation at the Hayflick sequence. However, this view appears to be very much overly-simplistic. Telomeres also appear to serve as a sort of "sink" for free radicals, such these molecules as well as other forms of cellular stress can result in shortening of the telomeres, possibly as a signal that damage has occurred. Additionally, if telomeres are regarded as an "aging clock" then neurons should never senesce, because they never divide! So, while research on telomeres and telomerase may prove extremely useful for addressing some forms of cancer and possibly some instances of cellular senesence, this research by no means appears to be any sort of holy grail for the development of life-extension therapies.

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