New ex vivo demyelination/remyelination models to defeat multiple sclerosis and neuromyelitis optica

yiting Liu

doi:10.4103/1673-5374.257525

摘要：Multiple sclerosis (MS) and neuromyelitis optica (NMO) are in-flammatory diseases of the central nervous system (CNS) resulting in CNS inflammation, infiltration of peripheral immune cells, loss of myelin and oligodendrocytes, interruption of axonal communi-cation, and neurologic deficits. Following oligodendrocyte injury, newly generated myelinating oligodendrocytes derived from oligo-dendrocyte progenitors (OPCs) may produce new myelin sheaths around denuded axons (remyelination) restoring neuronal function (Verden and Macklin, 2016). While remyelination is apparent in MS lesions, the process is often inefficient; in NMO, remyelination is even more limited. Currently, there are no restorative therapies for MS and NMO. Understanding the mechanisms underlying driving disease-specific myelin damage and repair is critical to identify re-myelination barriers and develop new treatments promoting remy-elination. Current studies to understand the molecular and cellular events regulating demyelination and remyelination processes have employed developmental, toxic, and caustic models of oligoden-drocyte injury. These models cannot replicate the inflammatory pa-thology of demyelination in MS and NMO, and fail to replicate the milieu that may inhibit repair (Plemel et al., 2017).