In an animal model of multiple sclerosis (MS), decreasing the amount of a protein (“Reelin”) (image) made in the liver significantly protected against development of the disease’s characteristic symptoms and promoted recovery in symptomatic animals, scientists the University of Texas Southwestern (UTSW) Medical Center report. The findings, published online on August 12, 2020 in Science Translational Medicine, could lead to a new treatment strategy for this neurological disease and other conditions marked by chronic inflammation. The article is titled “Reelin Depletion Protects Against Autoimmune Encephalomyelitis By Decreasing Vascular Adhesion Of Leukocytes.” In 1997, researchers discovered a protein secreted in the brain called “Reelin.” Subsequent work showed that Reelin appears to help the brain organize itself during development and assists in forming connections between brain cells during adulthood. However, as researchers learned more about Reelin, they discovered that large amounts of it are produced in the liver and that cells lining blood vessels have receptors for this protein. A 2016 study by Joachim Herz, MD, Director of the UTSW’s Center for Translational Neurodegeneration Research and Professor in the Departments of Molecular Genetics, Neurology and Neurotherapeutics, and Neuroscience at UTSW, and his colleagues showed that depleting levels of circulating Reelin protected mice from atherosclerosis. Probing deeper into the mechanism behind this phenomenon, the researchers found that Reelin appears to regulate the production of adhesion molecules on blood vessel walls that capture circulating monocytes, a type of inflammation-inducing immune cell.
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