Hi!
>While I agree short lived species are "behind" us in terms of
>evolving *solutions* to aging, aging itself is a fairly universal
>process (grey hair, reduced libido, organ failure, etc.) and so
>treatments or methods that work in short lived species would seem
>to be the first place to start in developing treatments for long
>lived species such as humans.
I'd say that the phenotype of aging in Drosophila, C. elegans and yeast
(three of the most used models) is different than that in humans. I think
it's likely (but not certain) that they age for different reasons than us.
As for studying Parkinson, it's the same old story of trying to minimize the
effects of aging instead of aiming at discovering what causes aging in the
first place. The NIA's funding policy is hardly helping us reach the fourth
millenium.
>Relatively sudden death syndromes, such as you point out in male
>marsupial mice, or the more common example of salmon, are probably
>stress induced death, perhaps with some of the characteristics of
>aging. They would be less likely to be good models in which to test
>aging interventions.
Not probably, certainly they are "stress induced death" (what I like to call
sexual intoxication); a phenotype quite different from human aging. However,
if you castrate the marsupial mice, they end up developing a senescence that
ressembles that in normal mice and even in humans (e.g. exponential increase
in mortaliy, diseases of the old age, etc.).
>I'd be in line for experimental procedures that have been demonstrated
>to extend the lifespan of mice to 5+ years. Even CR can't manage that
>accomplishment.
I'm interested in that too (mice's senescence is not much different than
human senescence).
Sorry for the late answer. Best wishes.
---
Joao Pedro de Magalhaes
The University of Namur (FUNDP)
Unit of Cellular Biochemistry & Biology
Rue de Bruxelles, 61
B-5000 Namur BELGIUM
Fax: + 32 81 724135
Phone: + 32 81 724133
Reason's Triumph: http://users.compaqnet.be/jpnitya/
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