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

Autor:	Guttenplan KA; Department of Neurobiology, School of Medicine, Stanford University, Stanford, 94305, CA, USA. kguttenp@stanford.edu.; Department of Genetics, School of Medicine, Stanford University, Stanford, 94305, CA, USA. kguttenp@stanford.edu., Weigel MK; Department of Neurobiology, School of Medicine, Stanford University, Stanford, 94305, CA, USA., Adler DI; Neuroscience Institute, NYU School of Medicine, New York, NY, 10016, USA., Couthouis J; Department of Genetics, School of Medicine, Stanford University, Stanford, 94305, CA, USA., Liddelow SA; Neuroscience Institute, NYU School of Medicine, New York, NY, 10016, USA.; Department of Neuroscience and Physiology, NYU School of Medicine, New York, NY, 10016, USA.; Department of Ophthalmology, NYU School of Medicine, New York, NY, 10016, USA., Gitler AD; Department of Genetics, School of Medicine, Stanford University, Stanford, 94305, CA, USA. agitler@stanford.edu., Barres BA; Department of Neurobiology, School of Medicine, Stanford University, Stanford, 94305, CA, USA.
Jazyk:	angličtina
Zdroj:	Nature communications [Nat Commun] 2020 Jul 27; Vol. 11 (1), pp. 3753. Date of Electronic Publication: 2020 Jul 27.
DOI:	10.1038/s41467-020-17514-9
Abstrakt:	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 SOD1 G93A ALS mouse model, providing evidence for gliosis as a potential ALS therapeutic target.
Databáze:	MEDLINE
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