Single gene deletion boosts lifespan

From Nature:

Life Researchers have created a mutant mouse that lives longer despite eating more and weighing less — all thanks to the loss of a single protein. Without this protein, the body is less susceptible to the heart-pounding effects of the hormone adrenaline, and may become more resistant to some forms of stress. Scientists are already developing drugs to inhibit this protein, called type 5 adenylyl cyclase (AC5). “Clearly we would be very interested in such a compound,” says cardiologist Stephen Vatner, who is part of the team that discovered this effect. 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.

Vatner, together with Junichi Sadoshima and other colleagues at the New Jersey Medical School at the University of Medicine and Dentistry of New Jersey in Newark, had initially set out to determine whether getting rid of AC5 leads to a healthier heart.

Drugs that block adrenaline signalling, called beta-blockers, are known to help patients who have had heart attacks or suffer from an irregular heartbeat. As the researchers revealed in 2003, mutant mice lacking 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, in a paper published in Cell this week2, they report that the treated mice lived 30% longer and did not develop the heart stress and bone deterioration that often accompanies ageing.

More here.