Reverse aging? Scientists find way to make old muscles young again

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It is a dream for everyone as they grow older to turn back the clock and live in a younger body once again.  While many have developed ways to make the body look younger cosmetically, there have been very few effective methods to combat the aging process within the body – until now.

For the first time ever, researchers have identified a crucial protein responsible for the decline of muscle repair and agility as the body ages.  Upon this discovery, the scientists were able to effectively halt muscle decline in mice, giving hope to similar treatments for humans in the future.

According to the study’s authors, loss of muscle strength and repair is one of the major concerns facing elderly citizens.

“A great advantage of medicine is that people are not dying as early as they used to, but the body hasn’t figured out how to maintain its muscle repair,” Andrew Brack, of the Massachusetts General Hospital Center for Regenerative Medicine and corresponding study author, told  “The average loss of muscle mass for the 80-year-old male is 40 percent.  Elderly people will fall over and break bones, they go to the hospital where they lose more muscle strength, and then don’t recover.”

Brack noted that muscle strength is also one of the main factors that keeps elderly individuals out of the hospital and allows them to be productive members of the workforce.  In order to combat this muscle decline, Brack and Albert Basson, who met at King’s College London, teamed up to see if they could put the process in reverse.

The key revolves around stem cells found within muscles.  During exercise or injury, these stem cells become activated and work fervently by dividing and multiplying into new muscle fibers that help to repair the muscle.  When they are no longer need, they retreat into a reservoir within the muscle and lay dormant until they are needed again.

The problem with aging muscles is that these ‘fixer’ stem cells don’t remain dormant when they’re not needed.  Instead, they become activated more and more and unnecessarily divide and multiply – causing them to die at a faster rate.  Since muscles only have a finite amount of these stem cells, the quicker the cells die, the less effective muscles become at repairing themselves.

Wondering exactly why the stem cells became more activated with age, Brack and Basson screened older muscles, finding higher levels of a protein called FGF2 – a protein that stimulates cell division.  The scientists figured these levels could explain the unnecessary cell activation.

“As your muscle gets old, you start making more of this FGF2 protein,” Basson, senior lecturer at King’s College London Dental Institute, told  “…When there’s more, the FGF2 starts waking up these stem cells and they start dividing.  The stem cells have a limited number of times they can divide before they die or differentiate into other cells.”

Basson figured that if they were able to boost a gene called SPRY2, which inhibits FGF2, then the stem cells would lay dormant until they were absolutely needed.  To test this theory, the researchers administered a common drug containing SPRY2 to suppress FGF2 levels in elderly mice.  Sure enough, the drugs halted the decline of muscle stem cells in the mice.

“We think of this as the first study where we’ve identified something that goes wrong in the aging muscle,” Basson said.  “There are a number of these FGF inhibitor drugs used in clinics for cancer, so they certainly can be given to patients.  But we’re still quite a ways off before we can think about using this drug.”

One major issue about suppressing FGF2 is that the protein is still necessary for activating stem cells when muscles encounter injury.  Because of this interesting paradox, Brack imagined a future drug containing SPRY2 that would be used during the least amount of physical exertion.

“I think the favorite expression is, ‘Too much of a good thing is a bad thing,’” Brack said. “…You couldn’t have someone on a drug like this forever – that would be very bad.  It would work in a timed-release manner – keeping FGF2 low in low demanding situations.  As we go through our daily lives as aged individuals, keep FGF low, but as we workout we want FGF to go up.”

With such encouraging results, coupled with the fact that FGF suppressant drugs are already on the market, Brack and Basson are eager to translate this idea into human therapies.  However, Brack cautioned not to view this as a way to increase lifespan, but more of a way to enhance living as we age.

“We don’t think in terms of longevity,” Brack said.  “Instead we want to know: how do we make it possible for an 80-year-old individual to run a marathon?  The purpose is not to live to 120, but to see how healthy and vital you can be.  That’s the future of regenerative medicine.”