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In our quest for the eternal answer to youth, science has responded by trying to determine certain biochemical and microbial factors that could be manipulated to stop the aging process, if not yet reverse it.

 Published in the journal Nature, for the first time ever, an international team of scientists from King's College London, Harvard University and Massachusetts General Hospital have stopped the aging process in the muscles of mice by manipulating the chemical components of a commonly used drug.

"Preventing or reversing muscle wasting in old age in humans is still a way off, but this study has for the first time revealed a process which could be responsible for age-related muscle wasting, which is extremely exciting," said Dr Albert Basson, Senior Lecturer at the King's College London Dental Institute in a statement.

Noting that muscle stem cells, which are principally responsible for repairing injury, become weaker with age and are unable to regenerate as fast or as strong, researchers discovered that the number of  dormant stem cells that are stored in every muscle (waiting to repair muscle damaged by injury or exercise) decreases as we get older.

Higher levels of a protein called FGF2 were found in the muscles of old mice, which was found to stimulate muscle cells to divide and, by discovery of unrelated research, was known to awaken the dormant pool of stem cells even when they are not needed.

By administering a common FGF2 inhibitor drug researchers were able to inhibit the decline in the number of muscle stem cells in the mice, which without intervention is usually kick-started into unnecessary action during the aging process.

The the discovery and progress is small in scale, researchers say that the findings provide clues as to how muscles lose mass with age, which can result in weakness that affects mobility and may cause falls.

"The finding opens up the possibility that one day we could develop treatments to make old muscles young again. If we could do this, we may be able to enable people to live more mobile, independent lives as they age," says Basson.

Next, researchers hope to analyze why FGF2 increases with age and hope to find a way to lower the production of the protein that could prevent rapid muscle loss and weakening.