Premyelinating oligodendrocytes in chronic lesions of multiple sclerosis.

By Ansi Chang, W. Tourtellotte, Richard A. Rudick, B. Trapp. New England Journal of Medicine, 2002

958 citations recorded by the source corpus.

Subfields: Developmental Neuroscience, Neurology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/d4fec55dbe33a93e34aabd033dc45d69aac253de

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In Developmental Neuroscience

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In Pathology and Forensic Medicine

Citations in the corpus

Myelin Impairs CNS Remyelination by Inhibiting Oligodendrocyte Precursor Cell Differentiation (2006, background): “However, for unknown reasons, the process may become arrested at the differentiation/ maturation phase, leaving lesions containing oligodendrocyte lineage cells but chronically demyelinated and vulnerable to progressive axonal degeneration (Wolswijk, 1998;Chang et al., 2000, 2002).”
New concepts in the immunopathogenesis of multiple sclerosis (2002, neutral): “These findings indicate that active oligodendrocytes might still be present even in chronic lesions, but do not succeed in remyelinating axon”
Multiple Sclerosis Pathology. (2018, background): “…determined by several factors, such as the presence of progenitor cells, their potential to differentiate into mature myelinating oligodendrocytes (Chang et al. 2002), the presence and functional properties of axons, and the occurrence of repeated demyelination of remyelinated areas (Bramow et…”
Dysregulation of the Wnt pathway inhibits timely myelination and remyelination in the mammalian CNS. (2009, background): “The finding of OLPs and premyelinating oligodendrocytes in chronic lesions of MS suggest that remyelination is most vulnerable during their differentiation rather than their recruitment (Wolswijk 1998; Chang et al. 2002; Kuhlmann et al. 2008).”
Why does remyelination fail in multiple sclerosis? (2002, background): “cgi?l=5354">PLP )-expressing pre-myelinating oligodendrocytes that have progressed to the stage of engaging demyelinated axons but have not progressed further to form compacted myelin sheath”
Remyelination is extensive in a subset of multiple sclerosis patients. (2006, background): “In some lesions, however, progenitor cells are abundantly present (Chang et al., 2000; Chang et al., 2002), but they may fail either because the axons are not permissive for remyelination (Charles et al., 2002) or the maturation of progenitor cells is inhibited (John et al., 2002).”
Developmental genetics of vertebrate glial–cell specification (2010, background): “For example, in multiple sclerosis and periventricular leukomalacia, markers (such as OLIG2) identified in developmental studies have been examined in neuropathological studies, showing that OPCs are blocked in their differentiation and fail to carry out normal repair functions after white-matter in”
Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis. (2008, background): “However, recent publications indicate that the number of OPCs is reduced over time in multiple sclerosis lesions (Chang et al., 2002; Reynolds et al., 2002; Wolswijk 2002; Wilson et al., 2006).”