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AC5 and Mouse Longevity
(Thursday July 26 2007)
 | Nature reports on a new longevity gene tweak: "Currently, the main focus of ageing research is on using calorie restriction as a way of activating a metabolic 'fountain of youth'. The new discovery, that knocking out a single cardiac gene could lengthen lifespan, was an unexpected byproduct of heart research. ... mutant mice lacking [the gene for protein] AC5 were more resistant to heart failure caused by pressure within the heart. But in the process, the research team also realised that the mutant mice lived longer than their normal counterparts. [Now] they report that the treated mice lived 30% longer and did not develop the heart stress and bone deterioration that often accompanies ageing. ... AC5 could boost longevity by reducing the trauma caused when chemically reactive forms of oxygen accumulate. The accrued damage from these molecules is thought to contribute to ageing. AC5 mutants make more of a protein called ERK2, which regulates oxidative-stress responses. When Vatner and his colleagues increased ERK2 levels in budding yeast, these yeast lived longer. There are several mysteries about the mice lacking AC5. Young mutants weigh the same as their normal counterparts, but elderly AC5 mutants weigh less - even though they eat more. That suggests a metabolic change [which] could be mimicking calorie restriction. It is also possible that mice without AC5 are more resistant to cancer." |
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