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Endogenous Neurogenesis, Oligodendrogenesis and Angiogenesis after Ischemic Brain Injury | OMICS International | Abstract
ISSN: 2155-9562

Journal of Neurology & Neurophysiology
Open Access

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Review Article

Endogenous Neurogenesis, Oligodendrogenesis and Angiogenesis after Ischemic Brain Injury

Toru Yamashita and Koji Abe*

Department of Neurology, Okayama University Graduate School of Medicine, Okayama, Japan

Corresponding Author:
Koji Abe
Department of Neurology
Okayama University Graduate School of Medicine
Okayama, Japan
Tel: +81-86-235-7365
Fax: +81-86-235-7368
E-mail: [email protected]

Received date: February 04, 2013; Accepted date: February 21, 2013; Published date: February 28, 2013

Citation: Yamashita T, Abe K (2013) Endogenous Neurogenesis, Oligodendrogenesis and Angiogenesis after Ischemic Brain Injury. J Neurol Neurophysiol S8:003. doi:10.4172/2155-9562.S8-003

Copyright: © 2013 Yamashita T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Since strokes are a major cause of death and result in a drastic reduction in the quality of life, a new strategy to minimize ischemic-related damage is thus required. Recent evidence indicates that endogenous neural stem cells of the subventricular zone give rise to not only neurons but also oligodendrocytes, which can restore a disrupted neuronal network in post-ischemic brain, and various kinds of neurotrophic factors, such as EGF, are known to promote this process. To promote the functional recovery of post-stroke brain, angiogenesis is also essential. It has been suggested that circulating endothelial progenitor cells (EPCs) can play an important role in angiogenesis of the post-stroke brain. The number or function of EPCs can also be modulated by various kinds of factors. For example, VEGF, G-CSF and statins can increase EPC levels. In this review, we discuss the present knowledge of endogenous neurogenesis/oligodendrogenesis/angiogenesis and how to enhance their ability to restore the neuronal network through self-repair strategies.