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TREM2 Promotes Microglial Survival by Activating Wnt/β-Catenin Pathway
Zheng H, Jia L, Liu CC, Rong Z, Zhong L, Yang L, Chen XF, Fryer JD et al.. The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017-01-11
Topic: Brain proteins, microglia and lab models
Triggering Receptor Expressed on Myeloid cells 2 (TREM2), which is expressed on myeloid cells including microglia in the CNS, has recently been identified as a risk factor for Alzheimer's disease (AD). TREM2 transmits intracellular signals through its transmembrane binding partner DNAX-activating protein 12 (DAP12). Homozygous mutations inactivating TREM2 or DAP12 lead to Nasu-Hakola disease; however, how AD risk-conferring variants increase AD risk is not clear.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Zheng, H., Jia, L., Liu, C. C., Rong, Z., Zhong, L., Yang, L., et al. (2017). TREM2 Promotes Microglial Survival by Activating Wnt/β-Catenin Pathway. The Journal of neuroscience : the official journal of the Society for Neuroscience. https://doi.org/10.1523/jneurosci.2459-16.2017
Vancouver
Zheng H, Jia L, Liu CC, Rong Z, Zhong L, Yang L, et al. TREM2 Promotes Microglial Survival by Activating Wnt/β-Catenin Pathway. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2017. doi:10.1523/jneurosci.2459-16.2017. PMID: 28077724.
BibTeX
@article{zheng2017-28077724,
author = {Zheng, H. and Jia, L. and Liu, C. C. and Rong, Z. and Zhong, L. and Yang, L. and Chen, X. F. and Fryer, J. D. and others},
title = {{TREM2 Promotes Microglial Survival by Activating Wnt/β-Catenin Pathway}},
journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
year = {2017},
doi = {10.1523/jneurosci.2459-16.2017},
pmid = {28077724},
url = {https://doi.org/10.1523/jneurosci.2459-16.2017}
}
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
- TREM2 transmits intracellular signals through its transmembrane binding partner DNAX-activating protein 12 (DAP12).
- Homozygous mutations inactivating TREM2 or DAP12 lead to Nasu-Hakola disease; however, how AD risk-conferring variants increase AD risk is not clear.
- To elucidate the signaling pathways underlying reduced TREM2 expression or loss of function in microglia, we respectively knocked down and knocked out the expression of TREM2 in in vitro and in vivo models.
- We found that TREM2 deficiency reduced the viability and proliferation of primary microglia, reduced microgliosis in Trem2 -/- mouse brains, induced cell cycle arrest at the G 1 /S checkpoint, and decreased the stability of β-catenin, a key component of the canonical Wnt signaling pathway responsible for maintaining many biological processes, including cell survival.
Why it matters
In lab-grown microglia and in mice lacking the Trem2 gene, losing TREM2 reduced how well the brain's immune cells (microglia) survived and multiplied, stalled them at an early stage of cell division, and made β-catenin, a protein in the Wnt signalling pathway, less stable. The authors conclude that TREM2 supports microglial survival through this pathway. This was not a study in people and tested no treatment, so it does not show that targeting TREM2 or Wnt/β-catenin helps with Alzheimer's disease.
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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, 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 (The Journal of neuroscience : the official journal of the Society for Neuroscience) |
| Journal's citation record | 4 / 4 | Journal of Neuroscience: journal h-index 651 (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 318 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 28.9 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 4 / 6 | Cited 11.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 42 other studies in this library |
| Still being cited | 3 / 4 | Cited 100 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 | 0 / 3 | Mayo Clinic in Florida: institution h-index 681 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28077724) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 52 / 100 | — |
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Read the original
- DOI: 10.1523/jneurosci.2459-16.2017
- PubMed: 28077724
- Original source →
- Free full text: Journal of Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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