Curie Brief
Turn on cookies to sign in
Signing in saves your progress to your Curie account. We can only do that with cookies on — turn them on to continue.
News
Scientists have cracked a key mystery of muscle aging. Researchers from Duke-NUS Medical School found that a gene called DEAF1 becomes overactive with age, disrupting muscle cells' ability to clear out damaged proteins. Exercise can restore this balance — but only up to a point, which may explain why some older adults benefit more from physical activity than others.
Scientists have long known that exercise helps aging muscles stay strong — now they know why. Researchers from Duke-NUS Medical School, Singapore General Hospital, and Cardiff University identified a gene called DEAF1 that becomes overactive as muscles age, throwing off a critical cellular maintenance system called mTORC1. When this system is out of balance, muscle cells produce proteins but fail to clear out damaged ones, leading to the gradual weakness and deterioration associated with aging.
The good news? Exercise can help fix it. Physical activity activates proteins that lower DEAF1 levels, restoring the balance between protein production and cleanup — essentially giving aging muscles a "reset." However, when DEAF1 levels become too elevated or protective proteins (FOXOs) fall too low, exercise alone may not be enough to fully restore muscle repair, potentially explaining why some older adults respond better to physical activity than others.
Published in PNAS and tested in fruit flies and mice, the findings open the door to potential therapies that could mimic exercise's molecular effects — especially for people who can't exercise due to surgery, illness, or chronic conditions like cancer.
Key Takeaways
Why it matters: Muscle loss affects millions of older adults, increasing fall risk, slowing recovery, and straining healthcare systems. Understanding the molecular mechanisms behind muscle aging could lead to new treatments that keep people stronger and more independent for longer.
