TREM2 variants: new keys to decipher Alzheimer disease pathogenesis
Colonna M, Wang Y.. Nature reviews. Neuroscience, 2016-02-25
Topic: Amyloid, tau and blood-test diagnosis
Genome-wide association studies have identified rare variants of the gene that encodes triggering receptor expressed on myeloid cells 2 (TREM2) - an immune receptor that is found in brain microglia - as risk factors for non-familial Alzheimer disease (AD). Furthermore, animal studies have indicated that microglia have an important role in the brain response to amyloid-β (Aβ) plaques and that TREM2 variants may have an impact on such a function. We discuss how TREM2 may control the microglial response to Aβ and its impact on microglial senescence, as well as the interaction of TREM2 with other molecules that are encoded by gene variants associated with AD and the hypothetical consequences of the cleavage of TREM2 from the cell surface.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Colonna, M., & Wang, Y. (2016). TREM2 variants: new keys to decipher Alzheimer disease pathogenesis. Nature reviews. Neuroscience. https://doi.org/10.1038/nrn.2016.7
Vancouver
Colonna M, Wang Y. TREM2 variants: new keys to decipher Alzheimer disease pathogenesis. Nature reviews. Neuroscience. 2016. doi:10.1038/nrn.2016.7. PMID: 26911435.
BibTeX
@article{colonna2016-26911435,
author = {Colonna, M. and Wang, Y.},
title = {{TREM2 variants: new keys to decipher Alzheimer disease pathogenesis}},
journal = {Nature reviews. Neuroscience},
year = {2016},
doi = {10.1038/nrn.2016.7},
pmid = {26911435},
url = {https://doi.org/10.1038/nrn.2016.7}
}
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Key findings
- Furthermore, animal studies have indicated that microglia have an important role in the brain response to amyloid-β (Aβ) plaques and that TREM2 variants may have an impact on such a function.
- We discuss how TREM2 may control the microglial response to Aβ and its impact on microglial senescence, as well as the interaction of TREM2 with other molecules that are encoded by gene variants associated with AD and the hypothetical consequences of the cleavage of TREM2 from the cell surface.
Why it matters
Genetic studies had linked rare variants of TREM2, an immune receptor on the brain's microglia, to a higher risk of non-familial Alzheimer's, and animal studies suggested these variants may change how microglia react to amyloid plaques. This 2016 review explores how TREM2 may control that response, its possible role in microglial ageing, its interactions with proteins made by other Alzheimer's risk genes, and the "hypothetical consequences" of TREM2 being cut from the cell surface. It reports no new data and proposes ideas to test, not a treatment.
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Study details
- Evidence strengthLow
How this study scored 50/100
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. We have no data on senior author's track record, so that was left out: it earned 48 of the 96 points we could judge it on, which is 50 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Nature reviews. Neuroscience) |
| Journal's citation record | 4 / 4 | Nature reviews. Neuroscience: journal h-index 572 (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 | 1 / 5 | 2016 — within 20 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 416 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 34.7 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 3 / 6 | Cited 4.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 60 other studies in this library |
| Still being cited | 3 / 4 | Cited 110 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| 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 26911435) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 48 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 48 of the 96 points we could judge it on is 50 out of 100. |
| Total | 50 / 100 | — |
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