Open AccessOligodendrocyte Pathophysiology and Treatment Strategies in Cerebral Ischemia
Author(s) -
Mifsud Gabriella,
Zammit Christian,
Muscat Richard,
Di Giovanni Giuseppe,
Valentino Mario
Publication year - 2014
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12263
Subject(s) - oligodendrocyte , white matter , neuroscience , glutamate receptor , myelin , ischemia , multiple sclerosis , medicine , hypoxia (environmental) , periventricular leukomalacia , stroke (engine) , excitotoxicity , oxidative stress , central nervous system , biology , receptor , immunology , magnetic resonance imaging , chemistry , oxygen , engineering , genetics , gestational age , radiology , pregnancy , mechanical engineering , organic chemistry
Summary Oligodendrocytes ( OL s), 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 OL s, 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 OL s in white matter ischemic injury and the current and emerging principles that form the basis for protective strategies against OL death.