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

Author

Listed:
  • Kevin A. Guttenplan

    (School of Medicine, Stanford University
    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
    NYU School of Medicine
    NYU School of Medicine)

  • Aaron D. Gitler

    (School of Medicine, Stanford University)

  • Ben A. Barres

    (School of Medicine, Stanford University)

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.

Suggested Citation

  • Kevin A. Guttenplan & Maya K. Weigel & Drew I. Adler & Julien Couthouis & Shane A. Liddelow & Aaron D. Gitler & Ben A. Barres, 2020. "Knockout of reactive astrocyte activating factors slows disease progression in an ALS mouse model," Nature Communications, Nature, vol. 11(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-17514-9
    DOI: 10.1038/s41467-020-17514-9
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    Cited by:

    1. Hyosung Kim & Kun Leng & Jinhee Park & Alexander G. Sorets & Suil Kim & Alena Shostak & Rebecca J. Embalabala & Kate Mlouk & Ketaki A. Katdare & Indigo V. L. Rose & Sarah M. Sturgeon & Emma H. Neal & , 2022. "Reactive astrocytes transduce inflammation in a blood-brain barrier model through a TNF-STAT3 signaling axis and secretion of alpha 1-antichymotrypsin," Nature Communications, Nature, vol. 13(1), pages 1-18, December.

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