Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 25, Issue 45, Pages 4755-4762Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612825666191216125725
Keywords
Multiple Sclerosis; neuroinflammation; oxidative stress; glial cross-talk; remyelination; microglia
Categories
Funding
- Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT)
- Fondo Nacional de Desarrollo Cientifico y Tecnologico (FONDECYT) [11160616]
- Programa de Cooperacion and Cooperacion Cientifica [ECOS 180013]
- [DIUA127-2018]
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Myelin is a specialized membrane allowing for saltatory conduction of action potentials in neurons, an essential process to achieve the normal communication across the nervous system. Accordingly, in diseases characterized by the loss of myelin and myelin forming cells -oligodendrocytes in the CNS-, patients show severe neurological disabilities. After a demyelinated insult, microglia, astrocytes and oligodendrocyte precursor cells invade the lesioned area initiating a spontaneous process of myelin repair (i.e. remyelination). A preserved hallmark of this neuroinflammatory scenario is a local increase of oxidative stress, where several cytokines and chemokines are released by ghat and other cells. This generates an environment that determines cell interaction resulting in oligodendrocyte maturity and the ability to synthesize new myelin. Herein we review the main features of the regulatory aspect of these molecules based on recent findings and propose new putative signal molecules involved in the remyelination process, focused in the etiology of Multiple Sclerosis, one of the main demyelinating diseases causing disabilities in the population.
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