As a natural part of ageing human muscles begin to shrink and become less strong, even during peak years. For some people the decline in muscle mass and function is excessive, this is called sarcopenia, and this condition is estimated to affect every third person over the age of 80 to reduce their mobility, autonomy, and quality of life.
The causes of sarcopenia are diverse running from altered muscle metabolism to changes in the nerves supplying muscles, now recent research has discovered that mTORC1 also contributes to the condition and its suppression with rapamycin slows the age-related muscle wasting.
“Contrary to our expectations, the long-term mTORC1 suppression with rapamycin is overwhelmingly beneficial for skeletal muscle aging in mice, preserving muscle size and strength,” says Daniel Ham, first author of the study. “Neuromuscular junctions, the sites where neurons contact muscle fibers to control their contraction, deteriorate during aging. Stable neuromuscular junctions are paramount to maintaining healthy muscles during aging and rapamycin effectively stabilizes them.” The researchers also demonstrate that permanently activating mTORC1 in skeletal muscle accelerates muscle ageing.
The scientists identified a molecular signature of sarcopenia with mTORC1 being the key driver. The user-friendly web application SarcoAtlas, which is supported by sciCORE, was developed to help the scientific community to further investigate how gene expression in skeletal muscle changes during the response to treatment with rapamycin or ageing.
Currently, there are no effective therapies to treat sarcopenia, these findings suggest that it is possible to slow down age-related muscle wasting with treatments that suppress mTORC1 which will extend the autonomy and quality of life of elderly populations.
