Demyelination and remyelination after spinal cord injury.
Since the discovery in the 1960s that remyelination can occur in the damaged central nervous system (CNS) (Bunge et al. 1961), there has been much progress in understanding the cellular and molecular biology of oligodendroglia and the factors that regulate their propagation, migration, differentiation, maturation, and ability to myelinate nerve axons. More recently, greater understanding of disease states and the role of oligodendrocytes in remyelination have sparked tremendous interest in this once obscure field. Although the explosion of information is being hampered by adherence to commonly held beliefs based on empirical evidence, novel molecular and cellular tools are allowing scientists to address age-old assumptions. It is now recognized that, as well as promoting salutatory conduction along axons, oligodendroglia are important near-term clinical targets for restoring function after CNS injury, particularly spinal cord injury. Thus, remyelination appears to be one of the most feasible restoration strategies. This review focuses on concepts that are important for developing strategies of repair. The brightest young scientists will be attracted into this exciting field by its near-term potential for human application.
McDonald
John W
JW
International Center for Spinal Cord Injury, Kennedy Krieger Institute and the Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. mcdonaldj@kennedykrieger.org
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D000818:Animals; D019070:Cell Lineage / Q000502:physiology; D003711:Demyelinating Diseases / Q000473:pathology*; D006801:Humans; D009416:Nerve Regeneration / Q000502:physiology*; D009457:Neuroglia / Q000502:physiology; D009836:Oligodendroglia / Q000502:physiology; D013118:Spinal Cord Diseases / Q000473:pathology / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000473:pathology* / Q000503:physiopathology