Multiple sclerosis (MS) is a debilitating disease in which the body’s own immune system attacks itself and can, over time, permanently destroy the protective sheaths, or myelin, around nerve fibers in the brain. Myelin insulates nerve cells and facilitates the transmission of messages along them. When the myelin sheath is damaged, the nerves themselves may become damaged, and patients experience a wide range of symptoms, including pain and fatigue, loss of vision, trouble walking, and in the most severe cases, loss of basic functions. Current therapies attempt to treat the disease by preventing or decreasing the frequency and intensity of autoimmune attacks, and by managing symptoms, but these treatments can’t repair the damage already done, and they often ultimately fail to prevent disease progression.
Research from Whitehead Institute Fellow Olivia Corradin and her laboratory provides new insights into the genetic risk factors and disease pathways that contribute to MS, and could eventually lead to new therapies for the disease. The findings appear in the journal Cell on dateTK in a paper co-first authored by Corradin lab researcher Anna Barbeau and Daniel Factor, currently a senior scientist at Convelo Therapeutics. The researchers investigated disease-associated DNA sequence changes called genetic variants—slight differences in the same DNA sequence that vary from person to person –that are risk factors for MS, meaning that people with those variants are more likely to develop the disease. Their key discovery was that immune cells are not the only cell types implicated in the development of MS; rather, genetic variants that affect cells in the central nervous system also appear to contribute to the disease, including variants that cause dysregulation in oligodendrocytes, the brain cells that produce myelin.
