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Knockout of reactive astrocyte activating factors slows disease progression in an ALS mouse model
Kevin A Guttenplan1,2, Maya K Weigel3, Drew I Adler4
1Department of Neurobiology, School of Medicine, Stanford University, Stanford, 94305, CA, USA. kguttenp@stanford.edu.
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.
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