"We are on the verge of a revolution in medicine: understanding, treating, and ultimately preventing the causes of degenerative aging. But medical revolutions only happen if we all stand up in support of funding and research. We did it for cancer. We're doing it for Alzheimer's. We can do it for aging - and create an era of longer, healthier lives!"

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    Thursday, November 26, 2009

    The Latest Rejuvenation Research: Volume 12, Number 5

    The latest issue of Rejuvenation Research, the journal chaired by biomedical gerontologist Aubrey de Grey, is available online. In this issue, Michael Fossel lays out the case for a focus on telomere biology:

    In 1990, telomere length was shown to correlate with cellular senescence; this discovery was followed by a series of papers affirming a causal relationship between telomere length and cell senescence. Further work demonstrated that telomere elongation reverses cellular senescnce in both cells and reconstituted human tissues. Since telomerase, the enzyme that elongates telomeres, is absent (or only transiently active) in normal human somatic cells, the result is a gradual decrease in telomere length with age in most human tissues. The implied potential for in vivo human telomere enlongation raises two critical clinical issues: (a) Does telomere shortening play a key role in human diseases and, if so, (2) is telomere enlongation an effective clinical intervention.

    You'll find a fair amount of material on telomere research back in the archives:

    Another paper in this Rejuvenation Research issue touches on the question of what the public at large thinks about engineered longevity and the prospects for living longer - which should inform our expectations for future fundraising initiatives. I'm inclined to think that money raised for research is a somewhat better metric than surveys for gaining an idea of the level of support that presently exists, but analysis of public sentiment isn't an area in which clear cut and useful answers tend to emerge. It is true, however, that fundraising for longevity science is enjoying far greater success than it has in past decades, even though we are still talking about tiny amounts in comparison to any established field.

    Despite speculations about likely public attitudes toward life extension, to date there have been few attempts to empirically examine the public's perspective of these issues. Using open-ended survey questions via telephone interviews, this study explored the attitudes of 605 members of the Australian public toward the implications of life extension. Participants were asked to briefly describe in their own words what they believed would be the beneficial, as well as negative, implications arising from life extension (if there were any), both for themselves personally and for society as a whole. Participants were also asked to describe any ethical concerns they had about life extension, if they had any at all. ... A considerable number of participants envisioned at least some beneficial as well as negative implications for themselves and for society, and many claimed to have at least some ethical concerns.

    Posted by Reason

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    Posted by: kurt9 at November 28, 2009 4:06 PM

    The problem I have with the telomere shortening theory of aging is that it cannot explain the aging of the slowly dividing tissues (brains, heart, etc.) as apposed to the more rapidly dividing tissue. I first heard about the telomere shortening theory of aging in the late 90's (about the time of the first mammalian cloning). I find it difficult to believe that this is a cause of aging.

    [Posted by: kurt9 at November 28, 2009 4:06 PM]

    Posted by: Jon_L at December 1, 2009 7:40 PM

    On the topic of telomeres, is telomerase responsible in any way for the negligible senescence of germ cells, as these must remain (genetically) intact through the sexual maturation and sexually active times of an organism (a good portion of the life span)? In my mind there must be some important factor involved in maintaining the purity of genes long enough to be passed along to combine and become those embryonic stem cells which hold so much promise in longevity research. Could (or is) telomerase responsible for this? And if so, how do they regulate it well enough to so rarely become cancerous?

    [Posted by: Jon_L at December 1, 2009 7:40 PM]

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