There might be some amount of repair that can happen to the myelin sheath.
Diseases such as multiple sclerosis are characterized by damage to the myelin sheath, a protective covering wrapped around nerve cells akin to insulation around an electrical wire. Researchers from Charité – Universitätsmedizin Berlin have discovered how the body initiates repair mechanisms to limit the extent of any damage to this sheath. Their findings, which provide a basis for the development of new drugs to treat multiple sclerosis, have been published in Nature Communications.
Charité’s research team decided to take a closer look at the body’s innate ability to heal itself, knowing that, under certain conditions, the central nervous system is capable of repairing damage to the myelin sheath. Specific molecular signals enable stem cells to differentiate into myelin repair cells (oligodendrocytes), which reside in a small stem-cell niche in the brain. Once they leave this niche, these repair cells migrate to where myelin damage has occurred in order to restore the affected nerve cells’ electrical insulation. Until now, very little had been known about the molecular signals responsible for initiating this myelin regeneration mechanism. “We have found that the Chi3l3 protein plays a central role in the body’s capacity to produce new myelin-forming oligodendrocytes,” says the study’s first author, Dr. Sarah-Christin Staroßom of Charité’s Institute for Medical Immunology. A researcher at the NeuroCure Cluster of Excellence and the Experimental and Clinical Research Center (ECRC), Dr. Staroßom explains the protein’s role as follows: “The Chi3l3 protein initiates the differentiation of neural stem cells into myelin repair cells, which restore the electrical insulation around damaged nerve cells.”
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