Multiple sclerosis (MS) is a chronic disease of the brain and spinal cord that is characterized by lesions called plaques. These plaques are focal areas in which the normal fatty covering of nerve fibers-myelin-has been lost. The loss of myelin, or demyelination, is believed to be mediated largely by an abnormal response of the patient's own immune system. Myelin serves as an insulating material for the nerve fibers, much like the plastic or rubber insulation on an electrical wire. When the myelin is destroyed, nerve fibers cannot conduct electrical signals between nerve cells (neurons) in the brain and spinal cord, thus resulting in the symptoms encountered in MS, such as weakness, abnormal sensations, difficulty walking, or loss of vision.

Our laboratory studies the cells that make myelin, called oligodendrocytes. These cells arise from precursor cells (OPCs) mostly during the early development of the human nervous system. However, some OPCs are present in the adult brain and spinal cord as well. Experimental evidence suggests that following an MS attack or flare-up, these OPCs can migrate to the area of demyelination, differentiate into mature oligodendrocytes, and remyelinate the damaged nerve fibers, thus helping to restore the patient's normal neurological function. In particular, we are interested in the molecular mechanisms that regulate the ability of OPCs to multiply and the proteins that mediate interactions between oligodendrocytes and nerve fibers. We hope that this information could be used someday to design new therapies to protect and repair myelin in patients with MS.