Neurological Diseases as Primary Gliopathies: A Reassessment of Neurocentrism

Author:

Verkhratsky Alexei123,Sofroniew Michael V.4,Messing Albee5,deLanerolle Nihal C.6,Rempe David7,Rodríguez José Julio238,Nedergaard Maiken9

Affiliation:

1. Faculty of Life Sciences, The University of Manchester, Manchester, U.K.

2. IKERBASQUE, Basque Foundation for Science, 48011, Bilbao, Spain

3. Department of Neurosciences, University of the Basque Country UPV/EHU, 48940, Leioa, Spain

4. Department of Neurobiology, David Geffen School of Medicine, University of California, 10833 Le Conte Avenue, Los Angeles, CA 90095-1763, U.S.A.

5. Department of Comparative Biosciences and Waisman Center, University of Wisconsin, 1500 Highland Avenue, Madison, WI 53705, U.S.A.

6. Department of Neurosurgery, FMB 414, PO Box 208082, New Haven, CT 06520-8082, U.S.A.

7. Center for Neural Development and Disease, Department of Neurology. University of Rochester Medical School, Rochester, NY 14580, U.S.A.

8. Institute of Experimental Medicine, ASCR, Videnska 1083, 142 20, Prague, Czech Republic

9. Division of Glia Disease and Therapeutics, Center for Translational Neuromedicine, Department of Neurosurgery, University of Rochester Medica School, Rochester, NY 14580, U.S.A.

Abstract

Diseases of the human brain are almost universally attributed to malfunction or loss of nerve cells. However, a considerable amount of work has, during the last decade, expanded our view on the role of astrocytes in CNS (central nervous system), and this analysis suggests that astrocytes contribute to both initiation and propagation of many (if not all) neurological diseases. Astrocytes provide metabolic and trophic support to neurons and oligodendrocytes. Here, we shall endeavour a broad overviewing of the progress in the field and forward the idea that loss of homoeostatic astroglial function leads to an acute loss of neurons in the setting of acute insults such as ischaemia, whereas more subtle dysfunction of astrocytes over periods of months to years contributes to epilepsy and to progressive loss of neurons in neurodegenerative diseases. The majority of therapeutic drugs currently in clinical use target neuronal receptors, channels or transporters. Future therapeutic efforts may benefit by a stronger focus on the supportive homoeostatic functions of astrocytes.

Publisher

SAGE Publications

Subject

Neurology (clinical),General Neuroscience

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