Oligodendrogenesis After Cerebral Ischaemia and Traumatic Brain Injury - European Medical Journal

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Oligodendrogenesis After Cerebral Ischaemia and Traumatic Brain Injury

Neurology
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Authors:
Zheng Gang Zhang,1 Michael Chopp1,2

1. Department of Neurology, Henry Ford Hospital, Detroit, Michigan, USA
2. Department of Physics, Oakland University, Rochester, Michigan, USA

Disclosure:

This work was supported by National Institutes of Health Grants RO1 NS075156 (ZGZ) and AG037506 (MC). The content is solely the responsibility of the authors and does not necessarily represent the official view of the National Institutes of Health.

Received:
07.10.13
Accepted:
25.10.13
Citation:
EMJ Neurol. ;1[1]:26-31. DOI/10.33590/emjneurol/10314620. https://doi.org/10.33590/emjneurol/10314620.
Keywords:
Cerebral ischaemia, traumatic brain injury, myelination, oligodendrocytes, oligodendrocyte progenitor cells

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.

Abstract

Stroke and traumatic brain injury (TBI) damage white and grey matter. Loss of oligodendrocytes and their myelin, impairs axonal function. Remyelination involves oligodendrogenesis during which new myelinating oligodendrocytes are generated by differentiated oligodendrocyte progenitor cells (OPCs). This article briefly reviews the processes of oligodendrogenesis in adult rodent brains, and promising experimental therapies targeting the neurovascular unit that reduce oligodendrocyte damage and amplify endogenous oligodendrogenesis after stroke and TBI.

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