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dc.contributor.authorMifsud, Gabriella
dc.contributor.authorZammit, Christian
dc.contributor.authorMuscat, Richard
dc.contributor.authorDi Giovanni, Giuseppe
dc.contributor.authorValentino, Mario
dc.identifier.citationMifsud, G., Zammit, C., Muscat, R., Di Giovanni, G., & Valentino, M. (2014). Oligodendrocyte pathophysiology and treatment strategies in cerebral ischemia. CNS Neuroscience & Therapeutics 20(7), 603-12.en_GB
dc.description.abstractOligodendrocytes (OLs), the myelin-forming cells of the central nervous system, form a functional unit with axons and play a crucial role in axonal integrity. An episode of hypoxia–ischemia causes rapid and severe damage to these particularly vulnerable cells via multiple pathways such as overactivation of glutamate and ATP receptors, oxidative stress, and disruption of mitochondrial function. The cardinal effect of OL pathology is demyelination and dysmyelination, and this has profound effects on axonal function, transport, structure, metabolism, and survival. The OL is a primary target of ischemia in adult-onset stroke and especially in periventricular leukomalacia and should be considered as a primary therapeutic target in these conditions. More emphasis is needed on therapeutic strategies that target OLs, myelin, and their receptors, as these have the potential to significantly attenuate white matter injury and to establish functional recovery of white matter after stroke. In this review, we will summarize recent progress on the role of OLs in white matter ischemic injury and the current and emerging principles that form the basis for protective strategies against OL death.en_GB
dc.publisherWiley-Blackwell Publishing Ltd.en_GB
dc.subjectHypoxia-Ischemia, Brainen_GB
dc.subjectOxidative stressen_GB
dc.subjectWhite matteren_GB
dc.titleOligodendrocyte pathophysiology and treatment strategies in cerebral ischemiaen_GB
dc.rights.holderThe copyright of this work belongs to the author(s)/publisher. The rights of this work are as defined by the appropriate Copyright Legislation or as modified by any successive legislation. Users may access this work and can make use of the information contained in accordance with the Copyright Legislation provided that the author must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the prior permission of the copyright holder.en_GB
dc.publication.titleCNS Neuroscience & Therapeuticsen_GB
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