A muscle-preserving therapy should be one day developed

A study at The University of Texas Health Science Center at San Antonio suggests that less protection from antioxidants and more damage from oxidative stress results in impairment to cells’ energy centers, which slowly leads to death of muscle cells.

It’s an inevitable process of aging called sarcopenia. Yes, at the big 40 men begin to lose muscle, and by age 80 up to a third of it may be gone.

The research team found that without a certain antioxidant enzyme to balance the formation of harmful reactive oxygen species (ROS), cellular energy centers called mitochondria fail to work properly. The mitochondria even add to the spate of ROS molecules and release factors leading to cell death. The impaired function of mitochondria has a detrimental effect on the way motor neurons ‘talk’ to the muscle to achieve muscle contraction. This interaction occurs at a specialized synapse where the nerve and muscle come in close contact. This key structure is called the neuromuscular junction.

Age-related muscle atrophy is a complex process and involves multiple systems. There are, however, common mechanisms occurring in sarcopenia and other neuromuscular diseases.

Researchers think that they should be able to gain insight that will help us to discover new therapeutic by understanding the mechanisms underlying age-related muscle atrophy and alterations at the neuromuscular junction.