Saving aging nerves from 'big eater' immune cells
Treatment that destroys macrophages rescues nerve fiber in aging mice
- Date:
- April 30, 2018
- Source:
- Society for Neuroscience
- Summary:
- Immune cells may contribute to weakness and mobility issues in the elderly by driving nerve degeneration, according to a study of aging mice and biopsies of human nerves. In mice, blocking a receptor necessary for the survival of these cells improved the structure of nerves and increased muscle strength.
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Immune cells may contribute to weakness and mobility issues in the elderly by driving nerve degeneration, according to a study of aging mice and biopsies of human nerves published in JNeurosci. In mice, blocking a receptor necessary for the survival of these cells improved the structure of nerves and increased muscle strength.
As populations live longer, it is increasingly important to minimize the impact of aging on quality of life. Breakdown of the nerves that link the brain and spinal cord to the rest of the body is commonly seen in the elderly and can additionally cause pain, often felt in the hands and feet.
Rudolf Martini and colleagues found the age-related damage to nerve myelin and axons was similar in both aging mice and humans. The femoral nerve of 24-month-old mice contained nearly three times as many macrophages, large immune cells whose name comes from the Greek for "big eaters," as those of 12- and 18-month-old mice. Treatment with a cytokine receptor inhibitor (developed and provided by Plexxikon Inc.) that causes macrophage death reduced this number by about 70% and restored the maximum grip force of the aging mice's hind legs to the levels of the 12-month-old mice.
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Materials provided by Society for Neuroscience. Note: Content may be edited for style and length.
Journal Reference:
- Xidi Yuan, Dennis Klein, Susanne Kerscher, Brian L. West, Joachim Weis, Istvan Katona, Rudolf Martini. Macrophage depletion ameliorates peripheral neuropathy in aging mice. The Journal of Neuroscience, 2018; 3030-17 DOI: 10.1523/JNEUROSCI.3030-17.2018
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