Demyelination as a rational therapeutic target for ischemic or traumatic brain injury
DOI
10.1016/j.expneurol.2015.03.017
Document Type
Journal Article
Publication Date
10-1-2015
Publication Title
Experimental Neurology
Volume
272
First Page
17
Last Page
25
ISSN
144886
Keywords
Cerebral ischemia, Demyelination, Oligodendrocyte, Remyelination, Traumatic brain injury
Abstract
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.
Open Access
Green Accepted
Preprint
Repository Citation
Shi, H., Hu, X., Leak, R., Shi, Y., An, C., Suenaga, J., Chen, J., & Gao, Y. (2015). Demyelination as a rational therapeutic target for ischemic or traumatic brain injury. Experimental Neurology, 272, 17-25. https://doi.org/10.1016/j.expneurol.2015.03.017