期刊
NEUROBIOLOGY OF AGING
卷 36, 期 5, 页码 1994-2003出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2015.02.019
关键词
TREM2; Prion disease; Neuroinflammation; Microglial activation; Pathogenesis
资金
- Advanced Grant of the European Research Council (ERC) [250356]
- European Union (NEURINOX) [278611]
- Swiss National Foundation (SNF) [31003A_141193, CRSI33_125073]
- Novartis Research Foundation
- Klinische Forschungsschwerpunkte (KFSPs) small RNAs and Human Hemato-Lymphatic Diseases
- Young Scientist Stipend of the Ernst-Jung foundation
- Swiss National Science Foundation (SNF) [31003A_141193, CRSI33_125073] Funding Source: Swiss National Science Foundation (SNF)
Dysfunctional variants of the innate immune cell surface receptor TREM2 (triggering receptor expressed on myeloid cells-2) were identified as major genetic risk factors for Alzheimer's disease and other neurodegenerative conditions. Here we assessed a possible involvement of TREM2 in prion disease. We report that TREM2 expression by microglia is significantly up-regulated upon prion infection. However, depletion of TREM2 did not affect disease incubation time and survival after intracerebral prion infection. Interestingly, markers of microglial activation were attenuated in prion-infected TREM2(-/-) mice, suggesting an involvement of TREM2 in prion-induced microglial activation. Further phenotype profiling of microglia revealed that TREM2 deficiency did not change microglial phenotypes. We conclude that TREM2 is involved in prion-induced microglial activation but does not noticeably modulate the pathogenesis of experimental prion infections. (C) 2015 Elsevier Inc. All rights reserved.
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