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Astrocytes-Friends or foes in multiple sclerosis?
Glia, 2007-10, Vol.55 (13), p.1300-1312
Williams, Anna
Piaton, Gabrièle
Lubetzki, Catherine
2007
Details
Autor(en) / Beteiligte
Williams, Anna
Piaton, Gabrièle
Lubetzki, Catherine
Titel
Astrocytes-Friends or foes in multiple sclerosis?
Ist Teil von
Glia, 2007-10, Vol.55 (13), p.1300-1312
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2007
Link zum Volltext
Quelle
Wiley Online Library Journals Frontfile Complete
Beschreibungen/Notizen
In multiple sclerosis (MS), the presence of demyelinating plaques has concentrated researchers' minds on the role of the oligodendrocyte in its pathophysiology. Recently, with the rediscovery of early and widespread loss of axons in the disease, new emphasis has been put on the role of axons and axon‐oligodendrocyte interactions in MS. Despite the fact that, in 1904, Müller claimed that MS was a disease of astrocytes, more recently, astrocytes have taken a back seat, except as the cells that form the final glial scar after all hope of demyelination is over. However, perhaps it is time for the return of the astrocyte to popularity in the pathogenesis of MS, with recent reports on the dual role of astrocytes in aiding degeneration and demyelination, by promoting inflammation, damage of oligodendrocytes and axons, and glial scarring, but also in creating a permissive environment for remyelination by their action on oligodendrocyte precursor migration, oligodendrocyte proliferation, and differentiation. We review these findings to try to provide a cogent view of astrocytes in the pathology of MS. © 2007 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0894-1491
eISSN: 1098-1136
DOI: 10.1002/glia.20546
Titel-ID: cdi_proquest_miscellaneous_68132888
Format
–
Schlagworte
Astrocytes
,
Axons
,
Cicatrix - etiology
,
demyelination
,
Humans
,
Inflammation - etiology
,
Multiple Sclerosis - complications
,
Multiple Sclerosis - pathology
,
Multiple Sclerosis - physiopathology
,
myelin
,
Myelin Sheath - pathology
,
Nerve Degeneration - etiology
,
Oligodendroglia - pathology
,
remyelination
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