ALTERATION IN OLIGODENDROGLIAL LINEAGE PROGRESSION FOLLOWING EXPOSURE TO BPA IN VITRO

Abstract

Multiple Sclerosis is an autoimmune disease characterized by demyelination and remyelination resulting in motor, sensory, visual, and autonomic dysfunctions that accumulate over time. Demyelination is thought to be caused by autoreactive lymphocytes that cross the highly regulated blood-brain barrier (BBB) made of cerebral endothelial cells. Oligodendrocytes in the central nervous system (CNS) synthesize myelin-related proteins, but a malfunction in the cell differentiation may contribute to improper myelination of the neuron or the inability to remyelinate after an autoimmune attack. A key environmental risk factor for MS is thought to be the widely used plasticizer bisphenol A (BPA). This study investigated the role on BPA as an etiologic agent of MS progression by investigating the changes induced in the OPC maturation cycle through BPA exposure at different concentrations. Quantification through differential immunohistochemical staining was analyzed by statistical tests.