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IFN-gamma enhances neurogenesis in wild-type mice and in a mouse model of Alzheimer's disease.

Authors
  • Baron, Rona
  • Nemirovsky, Anna
  • Harpaz, Idan
  • Cohen, Hagit
  • Owens, Trevor
  • Monsonego, Alon
Type
Published Article
Journal
The FASEB Journal
Publisher
Federation of American Society for Experimental Biology
Publication Date
Aug 01, 2008
Volume
22
Issue
8
Pages
2843–2852
Identifiers
DOI: 10.1096/fj.08-105866
PMID: 18390924
Source
Medline
License
Unknown

Abstract

The generation of new neurons and glia from a precursor stem cell appears to take place in the adult brain. However, new neurons generated in the dentate gyrus decline sharply with age and to an even greater extent in neurodegenerative diseases. Here we raise the question whether peripheral immune mechanisms can generate immunity to such deficits in neuronal repair. We demonstrate that in contrast to primarily innate immunity cytokines, such as interleukin-6 and tumor necrosis factor-alpha, the adaptive immunity cytokine IFN-gamma enhances neurogenesis in the dentate gyrus of adult mice and improves the spatial learning and memory performance of the animals. In older mice, the effect of IFN-gamma is more pronounced in both wild-type mice and mice with Alzheimer's-like disease and is associated with neuroprotection. In addition, IFN-gamma reverses the increase in oligodendrogenesis observed in a mouse model of Alzheimer's disease. We demonstrate that limited amounts of IFN-gamma in the brain shape the neuropoietic milieu to enhance neurogenesis, possibly representing the normal function of the immune system in controlling brain inflammation and repair.

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