Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Jun 12:8:145.
doi: 10.3389/fnins.2014.00145. eCollection 2014.

Oligodendrogenesis in the normal and pathological central nervous system

Bilal El Waly  1 , Magali Macchi  1 , Myriam Cayre  1 , Pascale Durbec  1
Affiliations
Review

Oligodendrogenesis in the normal and pathological central nervous system

Bilal El Waly et al. Front Neurosci. .

Abstract

Oligodendrocytes (OLGs) are generated late in development and myelination is thus a tardive event in the brain developmental process. It is however maintained whole life long at lower rate, and myelin sheath is crucial for proper signal transmission and neuronal survival. Unfortunately, OLGs present a high susceptibility to oxidative stress, thus demyelination often takes place secondary to diverse brain lesions or pathologies. OLGs can also be the target of immune attacks, leading to primary demyelination lesions. Following oligodendrocytic death, spontaneous remyelination may occur to a certain extent. In this review, we will mainly focus on the adult brain and on the two main sources of progenitor cells that contribute to oligodendrogenesis: parenchymal oligodendrocyte precursor cells (OPCs) and subventricular zone (SVZ)-derived progenitors. We will shortly come back on the main steps of oligodendrogenesis in the postnatal and adult brain, and summarize the key factors involved in the determination of oligodendrocytic fate. We will then shed light on the main causes of demyelination in the adult brain and present the animal models that have been developed to get insight on the demyelination/remyelination process. Finally, we will synthetize the results of studies searching for factors able to modulate spontaneous myelin repair.

Keywords: adult brain plasticity; mouse models; multiple sclerosis; myelin regeneration; oligodendrocyte; stem cells.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Abdel-Salam O. M., Khadrawy Y. A., Mohammed N. A., Youness E. R. (2012). The effect of gabapentin on oxidative stress in a model of toxic demyelination in rat brain. J. Basic Clin. Physiol. Pharmacol. 23, 61–68 10.1515/jbcpp-2012-0004 - DOI - PubMed
    1. Acs P., Komoly S. (2012). Selective ultrastructural vulnerability in the cuprizone-induced experimental demyelination. Ideggyogy. Sz. 65, 266–270 - PubMed
    1. Aguirre A., Dupree J. L., Mangin J. M., Gallo V. (2007). A functional role for EGFR signaling in myelination and remyelination. Nat. Neurosci. 10, 990–1002 10.1038/nn1938 - DOI - PubMed
    1. Aguirre A., Rizvi T. A., Ratner N., Gallo V. (2005). Overexpression of the epidermal growth factor receptor confers migratory properties to nonmigratory postnatal neural progenitors. J. Neurosci. 25, 11092–11106 10.1523/JNEUROSCI.2981-05.2005 - DOI - PMC - PubMed
    1. Aguirre A. A., Chittajallu R., Belachew S., Gallo V. (2004). NG2-expressing cells in the subventricular zone are type C-like cells and contribute to interneuron generation in the postnatal hippocampus. J. Cell Biol. 165, 575–589 10.1083/jcb.200311141 - DOI - PMC - PubMed

LinkOut - more resources