|
I should mention that there are any number of genetic tweaks and characteristics that cause shortened life span via something that may look a lot like accelerated degenerative aging (or some aspect of degenerative aging). Here's one example:
Aging is a highly complex biological process that is believed to involve multiple mechanisms. Mice that have small amounts of the mitotic checkpoint protein BubR1 age much faster than normal mice ... Our findings suggest that early onset of aging-associated phenotypes in mice with mitotic checkpoint gene defects is linked to cellular senescence and activation of the p53 and p16 pathways
While educational - there's no such thing as useless knowledge in biochemistry, as it will all be needed one day - this isn't really all that exciting. It doesn't demonstrate a mechanism that can extend life span. The body, or indeed any individual cell, is an enormously complex machine; a wide range of damaged, bad or missing components can cause it to grind to a halt far sooner than it otherwise might, and in ways that look very similar to the end fate of a fully functional, but old system.
With that in mind, here's a better discovery - a gene whose absence shortens life span, but is also associated with centenarians:
Perturbations in genomic stability result in cancer, a reduced life span, and premature aging. MLH1 is a mismatch repair enzyme that acts to maintain genomic stability, and a loss of MLH1 increases cancer incidence and apoptosis resistance, which suggests a link between MLH1 and longevity. We found here that MLH1 is associated with longevity by comparing a centenarian group with a control group. Our data indicate a critical role for MLH1 in longevity.
A nice demonstration that better DNA repair capabilities lead to a longer healthy life span, on average. You may be suffering age-related damage to your DNA, but your body is naturally better at repairing this damage.
Still, the same old comments apply - the demonstration is nice, but we already know a great deal about the association between DNA damage and age-related disease and degeneration. Tweaking a gene or its expression - by drugs or more advanced methods - won't get you very far in the grand scheme of things, even in the (at this time unlikely) case it does work to extend your healthy life span to match that of centenarians. So why spend time working towards that rather than working towards the capability to fix all forms of cellular damage far, far more efficiently that our present biochemistry?
Technorati tags: aging, longevity
|
|
Posted by Reason
|
|
|
|
