Researchers discover how the body initiates repair mechanisms that limit damage to the myelin sheath

Diseases such as multiple sclerosis are characterized by lesions of the "myelin sheath", a protective envelope wrapped around nerve cells and resembling insulation surrounding an electrical wire. Researchers at Charité – Universitätsmedizin Berlin have discovered how the body initiates repair mechanisms that will limit the extent of damage to the sheath. Their findings, which serve as a basis for the development of new drugs to treat multiple sclerosis, were published in the prominent journal Nature Communications.

Multiple sclerosis is the most common autoimmune disease of the central nervous system. Estimates suggest that more than 200,000 people are affected by the disease in Germany alone. People with multiple sclerosis suffer from visual and sensory problems, as well as disorders of coordination or even paralysis. These symptoms are caused by disruption of nerve impulses in the brain or spinal cord. This disruption occurs when the body's immune system attacks the myelin sheath, which wraps around the body's nerve fibers and provides electrical isolation. When the myelin sheath is no longer intact, communication between the nerve cells is impaired. Researchers around the world are looking for new ways to repair myelin sheath and, in doing so, seek to reduce neurological symptoms in people with multiple sclerosis. Charity researchers have now moved closer to this goal.

The Charity 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 able to repair the damage to the sheath of myelin. Specific molecular signals allow stem cells to differentiate into myelin repair cells (oligodendrocytes), which reside in a small stem cell niche in the brain. Once they have left this niche, these repair cells migrate to where myelin has been damaged in order to restore the electrical isolation of the affected nerve cells. Until now, very little was known about the molecular signals at the origin of the mechanism of myelin regeneration. "We have discovered that the Chi3l3 protein plays a central role in the body's ability to produce new oligodendrocytes that form myelin," says lead author of the study, Dr. Sarah-Christin Staroßom, of the Institute of Medical Immunology Charity. A researcher at the NeuroCure Excellence Center and the Center for Clinical and Experimental Research (CRCE), Dr. Staroßom explains the role of the protein as follows: "The Chi313 protein initiates the differentiation of neural stem cells into neural stem cells. myelin, which restore electrical insulation around damaged nerve cells ".

With the help of a mouse model, the research team was able to show that a reduction in Chi3l3 levels in the brain significantly alters the body's ability to produce oligodendrocytes, while a Chi3l3 infusion results in increased production of myelin repair cells. The same reaction was observed during an in vitro experiment using human cells. "We hope to use this knowledge to develop a new generation of drugs that can be used in the treatment of multiple sclerosis," says Dr. Staroßom. "In a next step, we will investigate in more detail whether Chi3l3 or related proteins can be used to reduce the neurological symptoms of multiple sclerosis patients."