title: Importance of oligodendrocyte protection, BBB breakdown and inflammation for remyelination.
abstract: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the CNS. A better understanding of why remyelination fails in MS is necessary to improve remyelination strategies. Remyelination is mediated by oligodendrocyte precursor cells (OPCs), which are widely distributed throughout the adult CNS. However, it is still unclear whether OPCs detectable in MS lesions survive the inflammatory response but are unable to myelinate or whether OPC and oligodendrocyte death is primarily responsible for remyelination failure and detectable OPCs enter demyelinated areas from adjacent tissue as the lesion evolves. Remyelination strategies should, therefore, focus on stimulation of differentiation or prevention of apoptosis, as well as establishment of a supportive environment for OPC-mediated remyelination, which may be especially important in chronically demyelinated lesions.
authors.affiliation: Departments of Neurology and Immunology, Mayo Clinic College of Medicine, 200 First Street, SW, Rochester, MN 55905, USA.
authors.forename: Jens
authors.initials: J
authors.lastname: Watzlawik
authors.forename: Arthur E
authors.initials: AE
authors.lastname: Warrington
authors.forename: Moses
authors.initials: M
authors.lastname: Rodriguez
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000503:physiopathology*; D016923:Cell Death / Q000502:physiology; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009103:Multiple Sclerosis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism; D009836:Oligodendroglia / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013234:Stem Cells / Q000502:physiology
chemical_list: D016207:Cytokines; D017382:Reactive Oxygen Species; D009569:Nitric Oxide