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Remyelination is the process of propagating oligodendrocyte precursor cells to form oligodendrocytes to create new myelin sheaths on demyelinated axons in the Central nervous system (CNS). This is a process naturally regulated in the body and tends to be very efficient in a healthy CNS. [ 1 ]
Myelinogenesis continues throughout the lifespan to support learning and memory via neural circuit plasticity as well as remyelination following injury. [2] Successful myelination of axons increases action potential speed by enabling saltatory conduction , which is essential for timely signal conduction between spatially separate brain regions ...
Glial scars rapidly form, and the glia actually produce factors that inhibit remyelination and axon repair; for instance, NOGO and NI-35. [ 6 ] [ 7 ] [ 8 ] The axons themselves also lose the potential for growth with age, due to a decrease in GAP43 expression, among others.
In addition, spontaneous remyelination does not appear to be rare, at least in the case of MS. Studies of MS lesions reported the average extent of remyelination as high as 47%. [53] Comparative studies of cortical lesions reported a greater proportion of remyelination in the cortex as opposed to white matter lesions. [50]
A repair process, called remyelination, takes place in early phases of the disease, but the oligodendrocytes are unable to completely rebuild the cell's myelin sheath. Repeated attacks lead to successively less effective remyelinations, until a scar-like plaque is built up around the damaged axons.
12568 Ensembl ENSG00000164885 ENSMUSG00000028969 UniProt Q00535 P49615 RefSeq (mRNA) NM_001164410 NM_004935 NM_007668 RefSeq (protein) NP_001157882 NP_004926 NP_031694 Location (UCSC) Chr 7: 151.05 – 151.06 Mb Chr 5: 24.62 – 24.63 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Cyclin-dependent kinase 5 is a protein, and more specifically an enzyme, that is encoded by the Cdk5 ...
These markers are specific for the different processes that drive the formation of plaques: inflammation, myelin breakdown, astrogliosis, oligodendrocyte injury, neurodegeneration, axonal loss and remyelination. MS lesions evolve differently during early versus chronic disease phases, and within each phase, different kind of activity appears.
Oligodendrocytes are a type of glial cell, non-neuronal cells in the central nervous system.They arise during development from oligodendrocyte precursor cells (OPCs), [8] which can be identified by their expression of a number of antigens, including the ganglioside GD3, [9] [10] [11] the NG2 chondroitin sulfate proteoglycan, and the platelet-derived growth factor-alpha receptor subunit (PDGF ...