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TREM2 in Neurodegenerative Diseases
Jay TR, von Saucken VE, Landreth GE.. Molecular neurodegeneration, 2017-08-02
Topic: Brain proteins, microglia and lab models
TREM2 variants have been identified as risk factors for Alzheimer's disease (AD) and other neurodegenerative diseases (NDDs). Because TREM2 encodes a receptor exclusively expressed on immune cells, identification of these variants conclusively demonstrates that the immune response can play an active role in the pathogenesis of NDDs. These TREM2 variants also confer the highest risk for developing Alzheimer's disease of any risk factor identified in nearly two decades, suggesting that understanding more about TREM2 function could provide key insights into NDD pathology and provide avenues for novel immune-related NDD biomarkers and therapeutics.
Key findings
- Because TREM2 encodes a receptor exclusively expressed on immune cells, identification of these variants conclusively demonstrates that the immune response can play an active role in the pathogenesis of NDDs.
- These TREM2 variants also confer the highest risk for developing Alzheimer's disease of any risk factor identified in nearly two decades, suggesting that understanding more about TREM2 function could provide key insights into NDD pathology and provide avenues for novel immune-related NDD biomarkers and therapeutics.
- The expression, signaling and function of TREM2 in NDDs have been extensively investigated in an effort to understand the role of immune function in disease pathogenesis and progression.
- We provide a comprehensive review of our current understanding of TREM2 biology, including new insights into the regulation of TREM2 expression, and TREM2 signaling and function across NDDs.
Why it matters
This 2017 review pulls together research on TREM2, a gene for a receptor found only on immune cells, whose variants are linked to a higher risk of Alzheimer's and other neurodegenerative diseases. The authors argue this shows the immune response can play an active part in these diseases, and say the variants carry the highest Alzheimer's risk of any risk factor found in the previous two decades. They suggest studying TREM2 could lead to new tests and immune-based treatments, but the review reports no new data and no treatment.
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Study details
- Evidence strengthLow
How this study scored 53/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular neurodegeneration) |
| Journal's citation record | 2 / 4 | Molecular Neurodegeneration: journal h-index 164 (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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 429 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 39.0 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 4 / 6 | Cited 15.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 56 other studies in this library |
| Still being cited | 3 / 4 | Cited 140 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Gary E. Landreth: h-index 101 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Case Western Reserve University: institution h-index 1,159 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28768545) |
| Free to read | 2 / 2 | Free to read |
| Total | 53 / 100 | — |
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Read the original
- DOI: 10.1186/s13024-017-0197-5
- PubMed: 28768545
- Original source →
- Free full text: Molecular Neurodegeneration →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Jay, T. R., von Saucken, V. E., & Landreth, G. E. (2017). TREM2 in Neurodegenerative Diseases. Molecular neurodegeneration. https://doi.org/10.1186/s13024-017-0197-5
Vancouver
Jay TR, von Saucken VE, Landreth GE. TREM2 in Neurodegenerative Diseases. Molecular neurodegeneration. 2017. doi:10.1186/s13024-017-0197-5. PMID: 28768545.
BibTeX
@article{jay2017-28768545,
author = {Jay, T. R. and von Saucken, V. E. and Landreth, G. E.},
title = {{TREM2 in Neurodegenerative Diseases}},
journal = {Molecular neurodegeneration},
year = {2017},
doi = {10.1186/s13024-017-0197-5},
pmid = {28768545},
url = {https://doi.org/10.1186/s13024-017-0197-5}
}
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