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TREM2 in CNS homeostasis and neurodegenerative disease
Painter MM, Atagi Y, Liu CC, Rademakers R, Xu H, Fryer JD, Bu G.. Molecular neurodegeneration, 2015-09-04
Topic: Brain proteins, microglia and lab models
Myeloid-lineage cells accomplish a myriad of homeostatic tasks including the recognition of pathogens, regulation of the inflammatory milieu, and mediation of tissue repair and regeneration. The innate immune receptor and its adaptor protein—triggering receptor expressed on myeloid cells 2 (TREM2) and DNAX-activating protein of 12 kDa (DAP12)—possess the ability to modulate critical cellular functions via crosstalk with diverse signaling pathways. As such, mutations in TREM2 and DAP12 have been found to be associated with a range of disease phenotypes.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Painter, M. M., Atagi, Y., Liu, C. C., Rademakers, R., Xu, H., Fryer, J. D., et al. (2015). TREM2 in CNS homeostasis and neurodegenerative disease. Molecular neurodegeneration. https://doi.org/10.1186/s13024-015-0040-9
Vancouver
Painter MM, Atagi Y, Liu CC, Rademakers R, Xu H, Fryer JD, et al. TREM2 in CNS homeostasis and neurodegenerative disease. Molecular neurodegeneration. 2015. doi:10.1186/s13024-015-0040-9. PMID: 26337043.
BibTeX
@article{painter2015-26337043,
author = {Painter, M. M. and Atagi, Y. and Liu, C. C. and Rademakers, R. and Xu, H. and Fryer, J. D. and Bu, G.},
title = {{TREM2 in CNS homeostasis and neurodegenerative disease}},
journal = {Molecular neurodegeneration},
year = {2015},
doi = {10.1186/s13024-015-0040-9},
pmid = {26337043},
url = {https://doi.org/10.1186/s13024-015-0040-9}
}
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 names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- The innate immune receptor and its adaptor protein—triggering receptor expressed on myeloid cells 2 (TREM2) and DNAX-activating protein of 12 kDa (DAP12)—possess the ability to modulate critical cellular functions via crosstalk with diverse signaling pathways.
- As such, mutations in TREM2 and DAP12 have been found to be associated with a range of disease phenotypes.
- In particular, mutations in TREM2 increase the risk for Alzheimer's disease and other neurodegenerative disorders.
- The leading hypothesis is that microglia, the resident immune cells of the central nervous system, are the major myeloid cells affected by dysregulated TREM2-DAP12 function.
Why it matters
This review states that mutations in TREM2 increase the risk for Alzheimer's disease and other neurodegenerative disorders and discusses TREM2 and DAP12 signaling. It reports no treatment, cure or prevention for Alzheimer's disease.
New to this subject? Start with our plain-English guide: Genetics →
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 randomized / 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 | 2015 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 169 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 13.0 citations a year over 13 year(s) since 2015 |
| Impact for its field and year | 3 / 6 | Cited 6.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 38 other studies in this library |
| Still being cited | 3 / 4 | Cited 50 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Guojun Bu: h-index 120 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Mayo Clinic: institution h-index 1,606 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 26337043) |
| Free to read | 2 / 2 | Free to read |
| Total | 50 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13024-015-0040-9
- PubMed: 26337043
- 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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