Recently there have been quite few discussions about the TOR pathways
causing aging.  While considering the molecular mechanisms which are
all related to cell "hyperstimulation" I cannot resist the thought
that the mediators in all these cases are the metabolites of
arachidonic acid (AA), i.e. eicosanoids.  Indeed their inhibitors
either derived from the Omega-3 fats or pharmaceuticals such as NSAIDs
help to alleviate the symptoms of age-related diseases.  Wouldn't it
be interesting to test whether AA-depletion has the same effects as
inhibiting the "hyper-functionality" by rapamycin?  Perhaps use the
EFAs during development but restrict them once the "aging" program
kicks in.  In EFAD state the body would manufacture its own PUFA
called Mead acid which doesn't have excessive signaling activity in
tissues.

Cell Cycle. 2006 Sep ;5 (18):2087-102 17012837
Aging and immortality: quasi-programmed senescence and its
pharmacologic inhibition.
Mikhail V Blagosklonny
While ruling out programmed aging, evolutionary theory predicts 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. Could it be switched off
pharmacologically? This would require identification of a molecular
target involved in cell senescence, organism aging 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, even though cell cycle is blocked. Is TOR
involved in organism aging? In fact, in yeast (where the cell is the
organism), 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,
'wear and tear', Hayflick limit, stem cell exhaustion) that play a
limited role now, when quasi-programmed senescence kills us first.
SOURCE: http://lib.bioinfo.pl/auth:Blagosklonny,MV

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