Deficiency of a single protein may drive muscle wasting in the elderly

Muscle wasting, also known as sarcopenia, is a large problem in our aging population. People typically lose about 1% of their muscle mass per year after the age of 50. One study in the US found the prevalence to be 36.5% in 4400 participants (average age of 70 years). Sarcopenia is a part of frailty syndrome, a common condition in elderly populations that puts them at greater risk of hospitalization, disability, or death. Currently there are no approved therapies for treating sarcopenia and there is a lack of understanding on the mechanism by which the muscle wasting occurs. However, using mice a group of researchers based in Spain have identified a single protein that decreases as the mice age and plays an important role in maintaining healthy muscle.

The protein of interest, mitofusin 2 (Mfn2), was found to be decreased in older mice and if you remove the protein in young mice you actually get gene patterns that look similar to those found in aging people. Additionally, when the researchers knocked out the protein in young mice, their muscle looked like, and behaved like the muscle from older mice. Mfn2 seems to be important in helping the body keep mitochondria healthy and in recycling mitochondria that are damaged beyond repair. By recycling the damaged mitochondria, the body can get rid of potentially damaging oxidants. In aging, a loss of Mfn2 could prevent the body from getting rid of damaged mitochondria resulting in damage and loss of the muscle. Interestingly, the young mice who that were missing Mfn2 were able to still recycling their damaged mitochondria, thanks to another group of proteins, but the older mice could not. This suggests that in elderly patients the other protective mechanisms that kick in when Mfn2 fails are also abnormal.

This work was done in mice and so it means that a potential treatment in humans is still a long way off. However, it offers a viable target for specifically treating sarcopenia in the elderly and perhaps by extension also frailty. Another study in humans suggested a decrease in Mfn2 in human populations but did not know the mechanism by which the muscle loss occurs. There is also hope that this treatment may be able to help in a severe form of muscle loss called cachexia that is often seen in patients with AIDS, COPD, and Cancer.

Image Credit: Mister G.C. Flickr 

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