Research has shown that the length of telomeres, which form a “cap” on the end of chromosomes, play a major role in aging. Shortened telomeres are a hallmark of many “premature aging” diseases. Several studies have shown exercise can preserve telomere length in humans, particularly as humans get older, and thus theoretically slow the aging process. Slowing aging is very different than actually reversing aging, however, but a recent study at Harvard has shown aging can indeed be reversed – in mice.
At Harvard, they bred genetically manipulated mice that lacked an enzyme called telomerase that stops telomeres getting shorter. Without the enzyme, the mice aged prematurely and suffered ailments, including a poor sense of smell, smaller brain size, infertility and damaged intestines and spleens. But when DePinho gave the mice injections to reactivate the enzyme, it repaired the damaged tissues and reversed the signs of ageing.
“These were severely aged animals, but after a month of treatment they showed a substantial restoration, including the growth of new neurons in their brains,” said DePinho.
You may be asking yourself, “If telomerase reverses aging, why aren’t we all taking regular telomerase injections?” While telomerase is very active in embryonic and infant humans, leading to rapid cell division, telomerase becomes less active in most cells as humans get older. As a result, the activation of telomerase in adults can cause these cells to become cancerous and lead to tumor growth. Mice, on the other hand, who continue to produce telomerase throughout their lifetimes, don’t appear to be subject to increased cancer risk.
The next steps for this study will measure whether the newly rejuvenated mice will live longer, healthier lives when compared with their control group brethren. Ultimately, while this study provides fascinating insights into one of the causes of aging, scientists have a long way to go before they might apply these findings toward practical anti-aging therapies for humans.
Merchants try to turn their stock quickly so that it doesn’t become stale, and, additionally, to ensure that there is room on the shelves to try out new products. There are some who have decided that living life to its fullest doesn’t include tricking the stock boy into letting them take up space on the shelf past the sell-by date. Regardless of belief system, there is no “better” to the outcome of dying later rather than sooner. Heavenly choirs or atoms scattered about, it will be what it will be, and that is the only certainty.
There is really no need for genetic engineering to activate telomerase as was done in the Depinho mouse model. There is about 20 years of research on Telomere activation. There are two receptors for estrogen on the TERT gene which controls this process. Whether you happen to be a human being or a mouse, the best way to increase telomerase activity, lengthen the telomeres and reverse aging is with the human bioidentical hormone, 17-Beta-Estradiol, also known as estrogen. In 1999, Kyo demonstrated that 17-Beta-Estradiol activates telomerase via direct and indirect effects on the hTERT promoter region. This was confirmed in 2000 by Silvia Misiti and again in 2009 by Rodrigo T. Calado from the NIH A recent December 2010 study from Imanishi from Japan showed that 17-Beta-Estradiol (estrogen) augments telomerase activity, thereby accelerating recovery after injury and reducing the effects of aging (reducing senescence). If this isn’t a description of anti-aging effects, I don’t know what is.
For more see:
http://jeffreydach.com/2010/12/03/anti-aging-breakthrough-with-telomerase-knockout-mice-by-jeffrey-dach-md.aspx
regards, jeffrey dach md