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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 FoxNews.com. “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 FoxNews.com. “…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.


Read more: Reverse aging? Scientists find way to make old muscles young again | Fox News