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Myelin is a specialized membrane, which wraps around axons in the peripheral (PNS) and central (CNS) nervous systems. In diseases such as Multiple Sclerosis (CNS) and Guillain-Barre Syndrome (PNS), loss of myelin around the nerve cells results in conduction block and underlies the clinical deficit characteristic of these disorders. Remyelination restores nerve conduction and leads to resolution of symptoms. However there are currently no treatments designed to directly target the efficiency of myelin repair and the return of nerve function. Our studies focus on the role of cytoskeletal signaling and its impact on myelinating glial cell differentiation, a fundamental knowledge that is currently lacking in the field.
There are two types of specialized myelin-forming glial cells: Schwann cells (SC) in the PNS, and oligodendrocytes (OL) in the CNS. We have found that a cytoskeletal protein: myosin II (MII) regulates the development of myelinating glial cells. MII inhibition impairs myelin formation by SC but enhances OL myelination. Our laboratory uses in vitro and in vivo models to elucidate the mechanisms behind these observations. We have the facilities and equipment necessary to purify and maintain primary cultures of rodent neurons and glia and to analyze their development using biochemistry, molecular biology, immunofluorescence and confocal microscopy. We recently generated conditional knockout mice to directly address the role of NMII on myelin formation and repair by SC and OL in vivo. Our long-term goal is to apply this knowledge to the development of novel therapeutic tools to treat demyelinating diseases.
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