Triggering receptor expressed on myeloid cells-2 is involved in prion-induced microglial activation but does not contribute to prion pathogenesis in mouse brains
Open accessAbstract
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.
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Although TREM2 is upregulated in murine and human prion diseases, it might not play a role in disease modification.
“Although TREM2 is upregulated in murine and human prion diseases, it might not play a role in disease modification [103,115].”
From Loss of Homeostatic Microglia Signature in Prion Diseases (2022) · cites this paper as [103]
Both ApoE and TREM2 are upregulated in prion disease and affect the expression of pro-inflammatory proteins during the disease course in murine models, but their depletion did not change survival times.
“Both proteins are upregulated in prion disease and affect the expression of pro-inflammatory proteins during the disease course in murine models. However, their depletion did not change survival times [102,103,104].”
From Loss of Homeostatic Microglia Signature in Prion Diseases (2022) · cites this paper as [103]
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- Authors
- Zhu, C., Herrmann, U. S., Li, B., Abakumova, I., Moos, R., Schwarz, P., Rushing, E. J., Colonna, M., & Aguzzi, A.
- Affiliations
- University Hospital Zurich (CH)
- Washington University in St. Louis (US)
- Corresponding author
- Zhu, Caihong
- Aguzzi, Adriano
- ORCID
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2015-05
- Volume
- 36
- Issue
- 5
- Pages
- 1994-2003
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W2016868102
- Cited by
- 44
- References
- 42
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 1 · 2022: 2 · 2021: 8 · 2020: 8 · 2019: 5 · 2018: 3 · 2017: 7 · 2016: 5
- FWCI
- 2.17
- Type
- journal article
- Language
- en
- Update notices
- erratum (2025-02-01)
- Open access
- bronze
- doi.org
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- European Research Council (250356)
- European Union (NEURINOX, No. 278611)
- Swiss National Foundation
- Novartis Research Foundation
- Klinische Forschungsschwerpunkte
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- TREM2, prion disease, microglial activation, prion pathogenesis, TREM2 knockout mice, TREM2 deficiency, innate immunity, neurodegeneration, Alzheimer's disease risk genes
- MeSH terms
- Animals, Membrane Glycoproteins, Mice, Transgenic, Phenotype, Receptors, Immunologic, Risk Factors, Up-Regulation, Gene Expression, Prion Diseases, Microglia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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