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Colony-stimulating factor 1 receptor (CSF1R) signaling in injured neurons facilitates protection and survival

Research output: Contribution to journalArticle

  • Jian Luo
  • Fiona Elwood
  • Markus Britschgi
  • Saul Villeda
  • Hui Zhang
  • Zhaoqing Ding
  • Liyin Zhu
  • Haitham Alabsi
  • Ruth Getachew
  • Ramya Narasimhan
  • Rafael Wabl
  • Nina Fainberg
  • Michelle L James
  • Gordon Wong
  • Jane Relton
  • Sanjiv S Gambhir
  • Jeffrey W Pollard
  • Tony Wyss-Coray

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    Rights statement: Copyright © 2013 Luo et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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    Licence: Creative Commons: Attribution-NonCommercial-ShareAlike (CC BY-NC-SA)

Original languageEnglish
Pages (from-to)157-72
Number of pages16
JournalJournal of Experimental Medicine
Issue number1
Publication statusPublished - 14 Jan 2013


Colony-stimulating factor 1 (CSF1) and interleukin-34 (IL-34) are functional ligands of the CSF1 receptor (CSF1R) and thus are key regulators of the monocyte/macrophage lineage. We discovered that systemic administration of human recombinant CSF1 ameliorates memory deficits in a transgenic mouse model of Alzheimer's disease. CSF1 and IL-34 strongly reduced excitotoxin-induced neuronal cell loss and gliosis in wild-type mice when administered systemically before or up to 6 h after injury. These effects were accompanied by maintenance of cAMP responsive element-binding protein (CREB) signaling in neurons rather than in microglia. Using lineage-tracing experiments, we discovered that a small number of neurons in the hippocampus and cortex express CSF1R under physiological conditions and that kainic acid-induced excitotoxic injury results in a profound increase in neuronal receptor expression. Selective deletion of CSF1R in forebrain neurons in mice exacerbated excitotoxin-induced death and neurodegeneration. We conclude that CSF1 and IL-34 provide powerful neuroprotective and survival signals in brain injury and neurodegeneration involving CSF1R expression on neurons.

    Research areas

  • Amyloid beta-Protein Precursor, Animals, Base Sequence, Cell Survival, Cognition, Cyclic AMP Response Element-Binding Protein, Disease Models, Animal, Humans, Interleukins, Kainic Acid, Macrophage Colony-Stimulating Factor, Mice, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data, Neurodegenerative Diseases, Neurons, Neuroprotective Agents, Phosphorylation, Prosencephalon, Receptor, Macrophage Colony-Stimulating Factor, Recombinant Proteins, Signal Transduction

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