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Altered microglial response to Aβ plaques in APPPS1-21 mice heterozygous for TREM2
Ulrich JD, Finn MB, Wang Y, Shen A, Mahan TE, Jiang H, Stewart FR, Piccio L et al.. Molecular neurodegeneration, 2014-06-03
Topic: Brain proteins, microglia and lab models
Background Recent genome-wide association studies linked variants in TREM2 to a strong increase in the odds of developing Alzheimer's disease. The mechanism by which TREM2 influences the susceptibility to Alzheimer's disease is currently unknown. TREM2 is expressed by microglia and is thought to regulate phagocytic and inflammatory microglial responses to brain pathology.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Ulrich, J. D., Finn, M. B., Wang, Y., Shen, A., Mahan, T. E., Jiang, H., et al. (2014). Altered microglial response to Aβ plaques in APPPS1-21 mice heterozygous for TREM2. Molecular neurodegeneration. https://doi.org/10.1186/1750-1326-9-20
Vancouver
Ulrich JD, Finn MB, Wang Y, Shen A, Mahan TE, Jiang H, et al. Altered microglial response to Aβ plaques in APPPS1-21 mice heterozygous for TREM2. Molecular neurodegeneration. 2014. doi:10.1186/1750-1326-9-20. PMID: 24893973.
BibTeX
@article{ulrich2014-24893973,
author = {Ulrich, J. D. and Finn, M. B. and Wang, Y. and Shen, A. and Mahan, T. E. and Jiang, H. and Stewart, F. R. and Piccio, L. and others},
title = {{Altered microglial response to Aβ plaques in APPPS1-21 mice heterozygous for TREM2}},
journal = {Molecular neurodegeneration},
year = {2014},
doi = {10.1186/1750-1326-9-20},
pmid = {24893973},
url = {https://doi.org/10.1186/1750-1326-9-20}
}
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
- The mechanism by which TREM2 influences the susceptibility to Alzheimer's disease is currently unknown.
- TREM2 is expressed by microglia and is thought to regulate phagocytic and inflammatory microglial responses to brain pathology.
- Given that a single allele of variant TREM2, likely resulting in a loss of function, conferred an increased risk of developing Alzheimer's disease, we tested whether loss of one functional trem2 allele would affect Aβ plaque deposition or the microglial response to Aβ pathology in APPPS1-21 mice.
- Results There was no significant difference in Aβ deposition in 3-month old or 7-month old APPPS1-21 mice expressing one or two copies of trem2.
Why it matters
Because a single copy of a TREM2 variant, "likely resulting in a loss of function", was linked to higher Alzheimer's risk, this study compared plaque-model mice (APPPS1-21) with one versus two working copies of the trem2 gene. It found "no significant difference in Aβ deposition" at 3 or 7 months of age; the title reports an altered microglial response to plaques, but this record does not describe that change. This is mouse work that tests no treatment, and the authors state that how TREM2 affects Alzheimer's risk was "currently unknown".
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Study details
- Evidence strengthLow
How this study scored 52/100
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 (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 | 1 / 5 | 2014 — 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 | Laboratory or animal study (title names “mice”) — 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 302 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 21.6 citations a year over 14 year(s) since 2014 |
| Impact for its field and year | 4 / 6 | Cited 11.0× 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 55 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 | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 24893973) |
| Free to read | 2 / 2 | Free to read |
| Total | 52 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/1750-1326-9-20
- PubMed: 24893973
- 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).
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