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TREM2 Function in Alzheimer's Disease and Neurodegeneration
Ulrich JD, Holtzman DM.. ACS chemical neuroscience, 2016-02-19
Topic: Brain proteins, microglia and lab models
Alzheimer's disease (AD), the most common cause of dementia in the elderly, is a complex neurodegenerative disease marked by the appearance of amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles. Alzheimer's disease has a strong genetic component, and recent advances in genome technology have unearthed novel variants in several genes, which could provide insight into the pathogenic mechanisms that contribute to AD. Particularly interesting are variants in the microglial-expressed receptor TREM2 which are associated with a 2-4-fold increased risk of developing AD.
Key findings
- Alzheimer's disease has a strong genetic component, and recent advances in genome technology have unearthed novel variants in several genes, which could provide insight into the pathogenic mechanisms that contribute to AD.
- Particularly interesting are variants in the microglial-expressed receptor TREM2 which are associated with a 2-4-fold increased risk of developing AD.
- Since the discovery of a link between TREM2 and AD, multiple studies have emerged testing whether partial or complete loss of TREM2 function contributed to Aβ deposition or Aβ-associated microgliosis.
- Although some confounding conflicting data have emerged from these studies regarding the role of TREM2 in regulating Aβ deposition within the hippocampus, the most consistent and striking observation is a strong decrease in microgliosis surrounding Aβ plaques in TREM2 haploinsufficient and TREM2 deficient mice.
Why it matters
This review reports that variants in the microglial-expressed receptor TREM2 are associated with a 2-4-fold increased risk of developing Alzheimer's disease. It summarizes research on whether loss of TREM2 function matters but offers no treatment or cure.
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Study details
- Evidence strengthLow
How this study scored 45/100
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 (ACS chemical neuroscience) |
| Journal's citation record | 1 / 4 | ACS Chemical Neuroscience: journal h-index 124 (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 | 5 / 7 | Cited 153 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 12.8 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 3 / 6 | Cited 7.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 24 other studies in this library |
| Still being cited | 2 / 4 | Cited 49 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 26854967) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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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
Ulrich, J. D., & Holtzman, D. M. (2016). TREM2 Function in Alzheimer's Disease and Neurodegeneration. ACS chemical neuroscience. https://doi.org/10.1021/acschemneuro.5b00313
Vancouver
Ulrich JD, Holtzman DM. TREM2 Function in Alzheimer's Disease and Neurodegeneration. ACS chemical neuroscience. 2016. doi:10.1021/acschemneuro.5b00313. PMID: 26854967.
BibTeX
@article{ulrich2016-26854967,
author = {Ulrich, J. D. and Holtzman, D. M.},
title = {{TREM2 Function in Alzheimer's Disease and Neurodegeneration}},
journal = {ACS chemical neuroscience},
year = {2016},
doi = {10.1021/acschemneuro.5b00313},
pmid = {26854967},
url = {https://doi.org/10.1021/acschemneuro.5b00313}
}
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