2015年10月
Demyelination as a rational therapeutic target for ischemic or traumatic brain injury
EXPERIMENTAL NEUROLOGY
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- 巻
- 272
- 号
- 開始ページ
- 17
- 終了ページ
- 25
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.expneurol.2015.03.017
- 出版者・発行元
- ACADEMIC PRESS INC ELSEVIER SCIENCE
Previous research on stroke and traumatic brain injury (TBI) heavily emphasized pathological alterations in neuronal cells within gray matter. However, recent studies have highlighted the equal importance of white matter integrity in long-term recovery from these conditions. Demyelination is a major component of white matter injury and is characterized by loss of the myelin sheath and oligodendrocyte cell death. Demyelination contributes significantly to long-term sensorimotor and cognitive deficits because the adult brain only has limited capacity for oligodendrocyte regeneration and axonal remyelination. In the current review, we will provide an overview of the major causes of demyelination and oligodendrocyte cell death following acute brain injuries, and discuss the crosstalk between myelin, axons, microglia, and astrocytes during the process of demyelination. Recent discoveries of molecules that regulate the processes of remyelination may provide novel therapeutic targets to restore white matter integrity and improve long-term neurological recovery in stroke or TBI patients. (C) 2015 Elsevier Inc. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/j.expneurol.2015.03.017
- ISSN : 0014-4886
- eISSN : 1090-2430
- PubMed ID : 25819104
- Web of Science ID : WOS:000364353700004