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LongeCity .                       Advocacy & Research for Unlimited Lifespans


Aging as continuation of development

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#1 opales

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Posted 03 October 2006 - 09:04 PM

New aging theory paper, which also describes an INTERVENTION TO THE KEY TOR PATHWAY WITH CURRENTLY EXISTING pharmaceutical, rapamycin (in fact, TOR=Target Of Rapamycin)

Blagosklonny MV.
Aging and Immortality: Quasi-Programmed Senescence and Its Pharmacologic
Cell Cycle. 2006 Sep 15;5(18) [Epub ahead of print]
PMID: 17012837 http://tinyurl.com/hwfmp
    Evolutionary theory predicts that, like aging cannot be programmed, a
program for development cannot be switched off in post-development. This
determines a quasi-program for aging, a continuation of the developmental
program that is not turned off, is constantly on, becoming hyper-functional
and damaging, causing diseases of aging.
Can it be switched off
pharmacologically? This would require a molecular target involved in cell
senescence, organism aging (senescence) and diseases of aging. Notably, cell
senescence is associated with activation of the TOR (target of rapamycin)
nutrient- and mitogen-sensing pathway, which promotes cell growth, while
cell cycle is blocked. Is the same pathway involved in organism aging? In
fact, in unicellular organisms (where cell and organism senescence merge),
caloric restriction, rapamycin and mutations that inhibit TOR all slow down
aging. In animals from worms to mammals caloric restrictions, life-extending
agents, and numerous mutations that increase longevity all converge on the
TOR pathway. And, in humans, cell hypertrophy, hyper-function and
hyperplasia, typically associated with activation of TOR, contribute to
diseases of aging. Theoretical and clinical considerations suggest that
rapamycin may be effective against atherosclerosis, hypertension and
hyper-coagulation (thus, preventing myocardial infarction and stroke),
osteoporosis, cancer, autoimmune diseases and arthritis, obesity, diabetes,
macula-degeneration, Alzheimer's and Parkinson's diseases.
Finally, I
discuss that extended life span will reveal new causes for aging (e.g., ROS,
'tear and wear', Hayflick limit, stem cell exhaustion) that play a limited
role now, when quasi-programmed senescence kills us first.

Although the below does not sound as promising at all

As with all immunosuppressive medications, rapamycin decreases the body's inherent anti-cancer activity and allows some cancers which would have been naturally destroyed to proliferate. Patients on immunosuppressive medications have a 10-100 x increased risk of cancer compared to the general population. Furthermore, patients currently have or have already been treated for cancer have a higher rate of tumor progression and recurrence than patients with an intact immune system.

Also see

Also interesting related news article

Edited by opales, 08 October 2006 - 08:02 PM.

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