Identifying, treating age-related muscle weakness
Friday, July 13, 2018
Lean muscle mass contributes up to 50 percent of total body weight in young adults, but that decreases to 25 percent by age 75 to 80. By 25 years of age, skeletal muscles have reached their maximum size.
Although the decrease in muscle tissue begins around the age of 50 years, the decrease becomes more dramatic after age 60 and results in diminished muscle function. This decline of muscle mass and strength, or sarcopenia, is often hastened by inactivity.
Aging and inactivity can be nearly crippling, causing general weakness, difficulty moving, stiffness, loss of balance, arthritis, and increased risk of injuries.
The peripheral nervous system, responsible for muscle and skin innervation, also has an increased risk of degenerating as people age. An estimated 20 million people in the United States have some form of peripheral neuropathy, a condition that develops because of damage to the peripheral nervous system, which transmits information between the central nervous system and every other part of the body.
Progressive muscle weakness has been evaluated in a new project conducted by Dr. Rudolf Martini, who heads the Section of Developmental Neurobiology at the Neurological Department of the Würzburg University Hospital.
Martini and his team of researchers evaluated an important aspect of age-related nerve degeneration that might be a target for therapy.
They systematically surveyed the changes occurring in the peripheral nerves of people aged 65 to 79 years, and observed an increased number of macrophages in the samples. While macrophages set inflammatory responses in motion, help heal wounds, and cleanse tissues, these cells also cause damage in some diseases.
The researchers thought that macrophages may also be involved in age-related nerve degeneration, so they evaluated the nerves of 24-month-old mice, noting that the age-related changes in the peripheral nerves in mice were similar to those in humans.
In both older humans and older mice, the number of macrophages was increased. Next, to test whether the increased macrophages were responsible for triggering the changes, the researchers added a substance to the mice’s food at 18 months, causing the macrophages to die off.
After six months of treatment, the team found that the age-related degeneration in the treated mice was much less pronounced. The mice had more muscular strength, and their motor endplates were in better shape than the uncontrolled mice.
This study shows that there is a causal relationship between inflammatory responses in aging nerves and the degenerative aging process, suggesting that treating age-related macrophage-induced inflammation may improve the structure and function of nerves, and increase mobility and quality of life.
In addition, the study implies that infections or age-related diseases, such as diabetes, may present an additional risk factor for aging nerves, indicating a need for further research and development of substances that target macrophages.
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