Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease that affects the central nervous system (CNS), particularly, in young adults. Current MS treatments aim to reduce demyelination; however, these have limited efficacy, display side effects and lack of regenerative activities. Oligodendrocyte progenitor cells (OPCs) represents the major source for new myelin. Upon demyelination, OPCs get activated, proliferate, migrate towards the lesion, and differentiate into remyelinating oligodendrocytes. Although myelin repair (remyelination) represents a robust response to myelin damage, during MS, this regenerative phenomenon decays in efficiency or even fails. CNS-resident pericytes (CNS-PCs) are essential for vascular homeostasis regulating blood-brain barrier (BBB) permeability and stability as well as endothelial cells (ECs) function during angiogenesis and neovascularization. Recent studies indicate that CNS-PCs also play a crucial role regulating OPC function during remyelination, and very importantly, these cells are substantially affected in MS. This chapter summarizes important aspects of MS and CNS remyelination as well as it provides new insights supporting the contribution of CNS-PCs to myelin regeneration and to MS pathology. Currently, there is evidence arguing in favor of CNS-PCs as novel therapeutic targets for the development of future treatments for MS.
Keywords: Blood-brain barrier; CNS-resident pericytes; Extracellular matrix; Multiple sclerosis; Neurovascular unit; Oligodendrocyte progenitor cells; Remyelination; Therapy.