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Study reveals enzyme linked to aging of spinal cord

  • 2 Min To Read
  • 7 months ago

A recent study led by the University of Chinese Academy of Sciences suggests that the degeneration of the spinal cord with age may be triggered by a protein called CHIT1. The researchers found that aged microglial cells, which are the primary immune cells of the central nervous system, displayed elevated expression of CHIT1 in cases of spinal cord degeneration. These microglial cells crowded around motor neurons, causing them to enter a state called "senescence," where they become old and can no longer replicate. This compromises their ability to function properly and leads to inflammation that damages nearby cells and tissue.

The researchers confirmed their findings through experiments using non-human primate models and a human motor-neuron cell culture model. They also discovered that treatment with ascorbic acid, also known as vitamin C, helped counteract the damaging effects of CHIT1-positive microglial cells on motor neurons. This treatment curbed cell senescence and attenuated neurodegeneration.

This research sheds light on the role of microglial cells in aging and motor neuron damage. The study used non-human primate models and human tissue samples, providing more accurate results compared to mouse models or simple cell cultures. The findings lay the groundwork for future research and open possibilities for the development of drugs to slow or reverse the degeneration of the spinal cord in older adults.

The implications of this research are significant, as spinal cord degeneration can result in impaired movement, muscle weakness, and a decrease in physical activity, ultimately affecting the quality of life for older adults. By identifying the protein CHIT1 as a potential target for drug development, there is hope for finding ways to mitigate the effects of aging on the spinal cord and improve overall musculoskeletal health.

Further research is needed to fully understand the mechanisms underlying the decline of motor neurons with age and to explore other potential targets for intervention. However, this study provides a promising step forward in the field of longevity and aging research, offering hope for future advancements in the treatment and prevention of age-related spinal cord degeneration.

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