Knockout of reactive astrocyte activating factors slows disease progression in an ALS mouse model

Kevin A. Guttenplan (), Maya K. Weigel, Drew I. Adler, Julien Couthouis, Shane A. Liddelow, Aaron D. Gitler () and Ben A. Barres
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Kevin A. Guttenplan: School of Medicine, Stanford University
Maya K. Weigel: School of Medicine, Stanford University
Drew I. Adler: Neuroscience Institute, NYU School of Medicine
Julien Couthouis: School of Medicine, Stanford University
Shane A. Liddelow: Neuroscience Institute, NYU School of Medicine
Aaron D. Gitler: School of Medicine, Stanford University
Ben A. Barres: School of Medicine, Stanford University

Nature Communications, 2020, vol. 11, issue 1, 1-9

Abstract: Abstract Reactive astrocytes have been implicated in the pathogenesis of neurodegenerative diseases, including a non-cell autonomous effect on motor neuron survival in ALS. We previously defined a mechanism by which microglia release three factors, IL-1α, TNFα, and C1q, to induce neurotoxic astrocytes. Here we report that knocking out these three factors markedly extends survival in the SOD1G93A ALS mouse model, providing evidence for gliosis as a potential ALS therapeutic target.

Date: 2020
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DOI: 10.1038/s41467-020-17514-9

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