Astrocytes are glial cells that play a crucial role in
providing a supportive environment for neurons, mainly by cell
cell
interactions mediating numerous physiological and
biochemical functions in the central nervous system (CNS).
Astrocytes are also critical for intercellular signaling in the
neurovascular unit. Although numerous reports have detailed the
complex effects of astrocytes upon neurons in neurodegenerative
disease, whether or not astrocytes act as initiators or contributors
in the pathogenesis of Amyotrophic Lateral Sclerosis (ALS)
remains unclear. A broad overview of astrocytes’ link to motor
neuron degeneration in ALS, as well as specific functions of
astrocytes within the neurovascular unit is presented. This review
summarizes current knowledge of the astrocyte’s role in disease
pathogenesis and discusses the potential of the astrocyte as a
target for future ALS therapies.
Open Access
Peer Reviewed
ISSN: 2378-8933
Neurological Research and Therapy
International open-access publishing for high-quality research, reviews, case studies, and scholarly communication.
Submit Manuscript
Original Research
Article in Press
The Role of Astrocytes in the Pathogenesis of Amyotrophic Lateral Sclerosis
Dimitri Falco1, David Eve1,2, Avery Thomson1 and Svitlana Garbuzova-Davis1-4*
Corresponding Author: Falco D, Eve D, Thomson A and Garbuzova-Davis S
Received: Apr 20, 2016
Accepted: May 01, 2017
Published: May 04, 2016
Views: 3
DOI: 10.14437
Abstract
Falco D, Eve D, Thomson A and Garbuzova-Davis S (2016) The Role of Astrocytes in the Pathogenesis of Amyotrophic
Lateral Sclerosis. Neurol Res Ther Open Access 3:114
Copyright:
Copyright: © 2016 NRTOA. This is an open-access article distributed under the terms of the Creative Commons Attribution License, Version 3.0, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and source are credited.
use, distribution, and reproduction in any medium, provided the original author and source are credited.
Indexed In
Google Scholar
DOAJ
PubMed
Scopus