A therapy to prevent muscles from deteriorating may not be far away, a US study seems to show. Human muscles begin to deteriorate by the age of 40 years. Now researchers might have discovered the route to the deterioration, and therein lies the hope.
Oxidative stress combined with lack of antioxidants results in impairment to cells' energy centers, which slowly leads to death of muscle cells.
In the absence of 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, say the scientists with the University of Texas Health Science Center at San Antonio.
"The impaired function of mitochondria also has a detrimental effect on the way motor neurons 'talk' to the muscle to achieve muscle contraction," said Holly Van Remmen, Ph.D., associate professor with the university's Barshop Institute for Longevity and Aging Studies and the Department of Cellular and Structural Biology. She co-ordinated the research.
Dr. Van Remmen said. "This interaction occurs at a specialized synapse where the nerve and muscle come in close contact." This key structure is called the neuromuscular junction, she said.
Youngmok C. Jang, Ph.D., a leading author in the study, investigated mice that were genetically engineered to lack an antioxidant enzyme called copper-zinc superoxide dismutase. He compared mitochondria from these mice and normal mice and found reduced function of the energy centers in the enzyme-deficient mice. This contributed to more cell death and muscle atrophy in the rodents. "As a result, their muscles were a lot smaller and weaker," Dr. Van Remmen said.
Insights gleaned about muscle loss can help scientists better understand other neuromuscular diseases such as amyotrophic lateral sclerosis (Lou Gehrig's disease). "Age-related muscle atrophy is a complex process and involves multiple systems," Dr. Van Remmen said. "There are, however, common mechanisms occurring in sarcopenia and other neuromuscular diseases. An understanding of the mechanisms underlying age-related muscle atrophy and alterations at the neuromuscular junction, we should be able to gain insight that will help us to discover new therapeutic interventions."
The paper was published online by The FASEB Journal
brought out by the Federation of American Societies for Experimental Biology.