Researchers have discovered the biological mechanism behind age-related loss of muscle strength and identified a drug that may help reverse this process.

As we age, our skeletal muscles tend to wither and weaken, a phenomenon known as sarcopenia which begins to appear at around age 40 and accelerates after 75.

This is a major cause of disability in the elderly and although exercise can help counter the effects of age-related muscle loss, there are no established treatments.

According to a new study by researchers at Columbia University Medical Centre published in Cell Metabolism, sarcopenia occurs when calcium leaks from a group of proteins in muscle cells called the ryanodine receptor channel complex.

Earlier work by the team leader, Dr Andrew Marks showed that leaks in these channels trigger a chain of events that ultimately limits the ability of muscle fibres to contract and contribute to Duchenne muscular dystrophy, a genetic disorder characterized by rapidly progressing muscle weakness and early death.

Since muscular dystrophy and sarcopenia have some commonalities, Dr Marks suspected that ryanodine receptor leakage may also be involved in age-related muscle loss, which the present study shows is the case.

“This is a completely new concept – that the damage that occurs in ageing is very similar to what happens in muscular dystrophy,” says Dr Marks, “thus as we age we essentially develop an acquired form of muscular dystrophy.”

The study also points to a possible therapy for sarcopenia: an experimental drug called S107, developed by Dr Marks and his colleagues. The drug acts by stabilizing calstabin1, a protein that binds to ryanodine receptors and prevents calcium leakage.

Source: Cell Metabolism
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