Diseases such as multiple sclerosis are characterized by damage to 'myelin sheath', a protector wrapped around nerve cells that is similar to insulation around an electrical cable. Researchers from Charite – Universitätsmedizin Berlin have discovered how the body starts a repair mechanism that will limit the level of damage to this sheath. Their findings, which provide the basis for the development of new drugs to treat multiple sclerosis, have been published in leading journals Nature Communication.
Multiple sclerosis is the most common autoimmune disease of the central nervous system. Estimates show that more than 200,000 people were affected by the disease in Germany alone. People with multiple sclerosis experience visual and sensory disorders, as well as coordination or even paralysis. These symptoms are caused by nerve impulse disorders both in the brain or spinal cord. This disorder occurs when the immune system attacks the myelin sheath, which is wrapped around the body's nerve fibers and provides electrical insulation. When the myelin sheath is no longer intact, communication between nerve cells is disrupted. Researchers around the world are looking for new ways to improve myelin sheaths and, by doing so, look for ways to reduce neurological symptoms in people with multiple sclerosis. Researchers from Charite have now moved a step closer to this goal.
The Charite 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 damage to the myelin sheath. Special molecular signals allow stem cells to differentiate into myelin repair cells (oligodendrocytes), which are in the small stem cell niche in the brain. Once they leave this niche, these repair cells migrate to where myelin damage has occurred to restore the electrical isolation of the affected nerve cells. Until now, very little was 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," said the study's first author, Dr. Sarah-Christin Staroßom from Charit's Institute for Medical Immunology. A researcher at the NeuroCure Cluster of Excellence and the Experimental and Clinical Research Center (ECRC), Dr. Staroßom explained the role of proteins as follows: "Chi3l3 proteins begin differentiation of neural stem cells into repair cells of myelin, which restore electrical isolation around damaged nerve cells."
Using a mouse model, the research team was able to show that a reduction in Chi3l3 levels in the brain significantly impaired the body's capacity for oligodendrocyte production, while infusion of Chi3l3 led to an increase in myelin repair cell production. The same reaction was observed during in vitro experiments using human cells. "We hope to use this knowledge to develop new generation drugs that can be used in the treatment of multiple sclerosis," explained Dr. Staroßom. "As a next step, we will study in more detail whether Chi3l3 or related proteins can be used to reduce neurological symptoms of patients with multiple sclerosis."
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