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

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作者
Kevin A. Guttenplan
Maya K. Weigel
Drew I. Adler
Julien Couthouis
Shane A. Liddelow
Aaron D. Gitler
Ben A. Barres
机构
[1] School of Medicine,Department of Neurobiology
[2] Stanford University,Department of Genetics
[3] School of Medicine,Department of Neuroscience and Physiology
[4] Stanford University,Department of Ophthalmology
[5] Neuroscience Institute,undefined
[6] NYU School of Medicine,undefined
[7] NYU School of Medicine,undefined
[8] NYU School of Medicine,undefined
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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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