Attempts to Overcome Remyelination Failure: Toward Opening New Therapeutic Avenues for Multiple Sclerosis

• Published in: Cellular and molecular neurobiology Vol. 37; no. 8; pp. 1335 - 1348
• Main Authors: Motavaf, Mahsa, Sadeghizadeh, Majid, Javan, Mohammad
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-11-2017; Springer Nature B.V
• Subjects: Animals; Anti-Inflammatory Agents - pharmacology; Anti-Inflammatory Agents - therapeutic use; Axons; Biomedical and Life Sciences; Biomedicine; Cell Biology; Central nervous system; Degeneration; Humans; Immunomodulation; Inflammation; Multiple sclerosis; Multiple Sclerosis - metabolism; Multiple Sclerosis - pathology; Multiple Sclerosis - therapy; Myelin; Myelin Sheath - drug effects; Myelin Sheath - metabolism; Myelin Sheath - pathology; Myelination; Nerve Regeneration - drug effects; Nerve Regeneration - physiology; Neurobiology; Neurosciences; Oligodendroglia - metabolism; Oligodendroglia - pathology; Remyelination - drug effects; Remyelination - physiology; Review Paper; Signal Transduction - drug effects; Signal Transduction - physiology; Remyelination failure; Myelin repair; Multiple sclerosis; Oligodendrocyte progenitor cells; Demyelination
• ISSN: 0272-4340; 1573-6830; 1573-6830
• DOI: 10.1007/s10571-017-0472-6

Multiple sclerosis (MS) is a chronic immune-mediated disorder of the central nervous system that results in destruction of the myelin sheath wrapped around the axons and eventual axon degeneration. The disease is pathologically heterogeneous; however, perhaps its most frustrating aspect is the lack of efficient regenerative response for remyelination. Current treatment strategies are based on anti-inflammatory or immunomodulatory medications that have the potential to reduce the numbers of newly evolving lesions. However, therapies are still required that can repair already damaged myelin for which current treatments are not effective. A prerequisite for the development of such new treatments is understanding the reasons for insufficient endogenous repair. This review briefly summarizes the currently suggested causes of remyelination failure in MS and possible solutions.