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Multiple sclerosis – helps cells to help themselves


Multiple Sclerosis - Helps cells to help themselves

Mice for the repair of myelin (oligodendrocytes) in the petri dish. These cells produce myelin (green), which they then use to repair myelin sheaths around the nerve cells. The blue color indicates the cores. Author: Staroßom / Charite

Diseases such as multiple sclerosis are characterized by the damage of the myelin envelope, and the protective coating wrapped around the nerve cells is similar to the insulation around the electric wire. Researchers from Charite – Universitatsmedizin Berlin have discovered that the body is launching repair mechanisms to limit any damage to this envelope. Their findings, which are the basis for the development of new drugs for the treatment of multiple sclerosis, were published in Nature Communications.

Multiple sclerosis is the most common autoimmune disease of the central nervous system. Estimates indicate that more than 200,000 people are affected by the disease only in Germany. People with multiple sclerosis have problems with vision and senses, as well as damage to coordination or even paralysis. These symptoms are caused by a disorder of the nerve impulses in the brain or spinal cord. This disorder occurs when the immune system of the organism attacks the lining of the myelin, which is wrapped around the nerve fibers of the body and provides electrical insulation. When the myelinic envelope is no longer intact, communication between the nerve cells is disturbed. Researchers around the globe are looking for new ways to repair the myelin envelope while trying to reduce neurological symptoms in people with multiple sclerosis. Researchers from Charite have now embarked on a decisive step closer to this goal.

The Charite Research Team decided to closely examine the innate ability of the organism to cure, knowing that, under certain conditions, the central nervous system was able to repair damage to the myelin envelope. Specific molecular signals allow the stem cells to differentiate into the cells for the repair of myelin (oligodendrocytes), which are found in a small niche of stem cells in the brain. Once they leave this niche, these repair cells migrate where there is damage to the myelin to restore the electrical isolation of the damaged nerve cells. So far, very little has been known about the molecular signals responsible for initiating this mechanism of regeneration of myelin. "We discovered that the Chi3l3 protein plays a central role in the body's ability to produce new oligodendroids that create myelin," says the first author of the study, Dr Sarah-Christin Oldfield of Charite's Institute of Medical Immunology. Researcher at the NeuroCure Cluster of Excellence and the Center for Experimental and Clinical Research (ECRC), dr. It explains the role of proteins in the following way: "Chi3l3 protein initiates the differentiation of nerve stem cells into myelin repair cells, which restore electrical isolation around damaged nerve cells."

Using the mouse model, the research team was able to demonstrate that reducing the level of Chi3l3 in the brain significantly reduces the ability of the oligodendrocyte production organism, while the infusion of Chi3l3 leads to an increase in the production of cell myelin repairs. 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," explains Dr. Staroßom. "As a next step, we will explore in more detail whether Chi3l3 or related proteins can be used to reduce neurological symptoms in patients with multiple sclerosis."

Researchers from MS find new ways to regenerate brain isolation

More information:
Sarah C. Staross and associates, Chi3l3 induces oligodenrogenesis in an experimental autoimmune neuroinflammatory model, Nature Communications (2019). DOI: 10.1038 / s41467-018-08140-7

Charite – Universitatsmedizin Berlin

Multiple sclerosis – helps cells to help themselves (2019, January 23)
taken on January 23, 2019
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