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TREM2 deficiency attenuates neuroinflammation and protects against neurodegeneration in a mouse model of tauopathy
Leyns CEG, Ulrich JD, Finn MB, Stewart FR, Koscal LJ, Remolina Serrano J, Robinson GO, Anderson E et al.. Proceedings of the National Academy of Sciences of the United States of America, 2017-10-09
Topic: Brain proteins, microglia and lab models
Variants in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) were recently found to increase the risk for developing Alzheimer's disease (AD). In the brain, TREM2 is predominately expressed on microglia, and its association with AD adds to increasing evidence implicating a role for the innate immune system in AD initiation and progression. Thus far, studies have found TREM2 is protective in the response to amyloid pathology while variants leading to a loss of TREM2 function impair microglial signaling and are deleterious.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Leyns, C. E. G., Ulrich, J. D., Finn, M. B., Stewart, F. R., Koscal, L. J., Remolina Serrano, J., et al. (2017). TREM2 deficiency attenuates neuroinflammation and protects against neurodegeneration in a mouse model of tauopathy. Proceedings of the National Academy of Sciences of the United States of America. https://doi.org/10.1073/pnas.1710311114
Vancouver
Leyns CEG, Ulrich JD, Finn MB, Stewart FR, Koscal LJ, Remolina Serrano J, et al. TREM2 deficiency attenuates neuroinflammation and protects against neurodegeneration in a mouse model of tauopathy. Proceedings of the National Academy of Sciences of the United States of America. 2017. doi:10.1073/pnas.1710311114. PMID: 29073081.
BibTeX
@article{leyns2017-29073081,
author = {Leyns, C. E. G. and Ulrich, J. D. and Finn, M. B. and Stewart, F. R. and Koscal, L. J. and Remolina Serrano, J. and Robinson, G. O. and Anderson, E. and others},
title = {{TREM2 deficiency attenuates neuroinflammation and protects against neurodegeneration in a mouse model of tauopathy}},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
year = {2017},
doi = {10.1073/pnas.1710311114},
pmid = {29073081},
url = {https://doi.org/10.1073/pnas.1710311114}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- In the brain, TREM2 is predominately expressed on microglia, and its association with AD adds to increasing evidence implicating a role for the innate immune system in AD initiation and progression.
- Thus far, studies have found TREM2 is protective in the response to amyloid pathology while variants leading to a loss of TREM2 function impair microglial signaling and are deleterious.
- However, the potential role of TREM2 in the context of tau pathology has not yet been characterized.
- In this study, we crossed Trem2 +/+ (T2 +/+ ) and Trem2 -/- (T2 -/- ) mice to the PS19 human tau transgenic line (PS) to investigate whether loss of TREM2 function affected tau pathology, the microglial response to tau pathology, or neurodegeneration.
Why it matters
Researchers bred mice that develop human tau pathology (the PS19 line) to have either normal Trem2 or no Trem2 at all, because TREM2's role "in the context of tau pathology has not yet been characterized." The paper's title reports that losing TREM2 "attenuates neuroinflammation and protects against neurodegeneration" in these mice, the reverse of earlier amyloid studies, where TREM2 was "protective". This is a gene-knockout experiment in mice, not a treatment, and our stored record does not include the detailed results.
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Study details
- Evidence strengthLow
How this study scored 56/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Proceedings of the National Academy of Sciences of the United States of America) |
| Journal's citation record | 4 / 4 | Proceedings of the National Academy of Sciences: journal h-index 1,167 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2017 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “mouse”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 514 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 46.7 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 4 / 6 | Cited 16.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 95 other studies in this library |
| Still being cited | 3 / 4 | Cited 144 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author David M. Holtzman: h-index 206 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Washington University in St. Louis: institution h-index 1,962 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29073081) |
| Free to read | 2 / 2 | Free to read |
| Total | 56 / 100 | — |
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Read the original
- DOI: 10.1073/pnas.1710311114
- PubMed: 29073081
- Original source →
- Free full text: Proceedings of the National Academy of Sciences →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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