Abstract: MS is an irreversible and progressive central nervous system (CNS) disease which originates in the autoimmune attack of lymphocytes against CNS myelin. This specialized membrane, synthesized by oligodendrocytes (OL) in the CNS, provides metabolic support to axons and allows for saltatory conduction in neurons. The lack of myelin (i.e., demyelination) leads to axonal degeneration, neuronal death, and the consequent neurological disabilities (Franklin and Ffrench-Constant, 2017). Although the causes of MS are still matter of active investigation, the early events preceding the demyelination onset have been characterized in deep. Evidence indicates that there is an increase in the blood-brain barrier (BBB) permeability, followed by the infiltration of CD4+ T lymphocytes, which, in turn, induces the overactivation of microglia and astrocytes present in the white matter. The latter leads to the dysregulation of the inflammatory response, being characterized by an increased concentration of proinflammatory cytokines promoting myelin loss (recently reviewed in Varas and Ortiz, 2019).