The cellular and molecular events of central nervous system remyelination
Identifieur interne : 001C20 ( Main/Exploration ); précédent : 001C19; suivant : 001C21The cellular and molecular events of central nervous system remyelination
Auteurs : Monique Dubois-Dalcq [États-Unis] ; Regina Armstrong [États-Unis]Source :
- BioEssays [ 0265-9247 ] ; 1990-12.
English descriptors
- Teeft :
- Adult progenitors, Adult rats, Adult rodent, Animal models, Astrocyte, Autopsy tissue, Axon, Axonal membrane, Briefly review, Cell receptor, Cell type, Cellular events, Cgrp research, Craig jordan, Cultured oligodendrocytes, Demyelinated, Demyelinated lesions, Demyelinating, Demyelinating disease, Demyelinating episode, Demyelinating lesions, Demyelinating tissue, Demyelination, Efficient remyelination, Experimental models, Glial, Glial cells, Glial fibrillary acidic protein, Growth factor, Growth factors, Human demyelinating diseases, Internode, Lesion, Lesioned areas, Lineage, Lineage cell, Lineage cells, Mature oligodendrocytes, Mitogenic, Mitogenic signals, Molecular events, Monoclonal antibody, Multiple sclerosis, Murine, Murine hepatitis virus strain, Myelin, Myelin gene transcripts, Myelin internodes, Myelin regeneration, Myelin repair, Myelin sheath, Myelinated, Neonatal, Nerve impulses, Nervous system, Neuron, Oligodendrocyte, Oligodendrocyte lineage, Oligodendrocyte precursor cells, Oligodendrocyte proliferation, Oligodendrocyte regeneration, Optic nerve, Phase contrast, Phenotype, Phenotype cells, Plenum press, Precursor, Precursor cells, Present evidence, Present time, Progenitor, Progenitor cells, Protein transcripts, Recent studies, Regeneration, Remyelination, Schwann cells, Sclerosis, Spinal, Spinal cord, White matter.
Abstract
Central nervous system (CNS) Abbreviations: CNS=central nervous system; PNS=peripheral nervous system; MS=multiple sclerosis; MBP=myelin basic protein; MHC=major histocompatibility complex; EAE=experimental allergic encephalomyelitis; O‐2A=oligodendrocyte‐type 2 astrocyte; GC=galactocerebroside; GFAP=glial fibrillary acidic protein; FGF=fibroblast growth factor; IGF1=insulin‐like growth factor. regeneration is a subject of great interest, particularly in diseases causing a dramatic loss of neurons. However, some CNS diseases do not affect neurons but damage other cells, such as the myelin‐forming cells — called oligodendrocytes — which are also crucial to the harmonious function of the nervous system. Diseases in which oligodendrocytes and myelin are attacked can cause devastating neurological dysfunction which is sometimes followed by recovery and myelin repair or remyelination. The question of the regeneration potential of oligodendrocytes in experimental and human demyelinating diseases such as multiple sclerosis has been debated for a long time. Present evidence suggests that oligodendrocyte precursor cells persist in the adult CNS and that oligodendrocyte regeneration can occur but may be limited by ongoing disease processes. Here we will briefly review recent advances which have broadened our understanding of the cellular and molecular events of CNS remyelination.
Url:
DOI: 10.1002/bies.950121203
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Central nervous system (CNS) Abbreviations: CNS=central nervous system; PNS=peripheral nervous system; MS=multiple sclerosis; MBP=myelin basic protein; MHC=major histocompatibility complex; EAE=experimental allergic encephalomyelitis; O‐2A=oligodendrocyte‐type 2 astrocyte; GC=galactocerebroside; GFAP=glial fibrillary acidic protein; FGF=fibroblast growth factor; IGF1=insulin‐like growth factor. regeneration is a subject of great interest, particularly in diseases causing a dramatic loss of neurons. However, some CNS diseases do not affect neurons but damage other cells, such as the myelin‐forming cells — called oligodendrocytes — which are also crucial to the harmonious function of the nervous system. Diseases in which oligodendrocytes and myelin are attacked can cause devastating neurological dysfunction which is sometimes followed by recovery and myelin repair or remyelination. The question of the regeneration potential of oligodendrocytes in experimental and human demyelinating diseases such as multiple sclerosis has been debated for a long time. Present evidence suggests that oligodendrocyte precursor cells persist in the adult CNS and that oligodendrocyte regeneration can occur but may be limited by ongoing disease processes. Here we will briefly review recent advances which have broadened our understanding of the cellular and molecular events of CNS remyelination.</div>
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