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Amyloid-beta modulates microglial responses by binding to the triggering receptor expressed on myeloid cells 2 (TREM2)
Zhong L, Wang Z, Wang D, Wang Z, Martens YA, Wu L, Xu Y, Wang K et al.. Molecular neurodegeneration, 2018-03-27
Topic: Brain proteins, microglia and lab models
Background TREM2 is an innate immune receptor specifically expressed in microglia. Coding variations in TREM2 have been reported to increase the risk for Alzheimer's disease (AD) and other neurodegenerative diseases. While multiple studies support a role for TREM2 in microglial recruitment to amyloid plaques, the chemoattractant factor modulating TREM2-dependent microglial responses has not been defined.
Key findings
- Coding variations in TREM2 have been reported to increase the risk for Alzheimer's disease (AD) and other neurodegenerative diseases.
- While multiple studies support a role for TREM2 in microglial recruitment to amyloid plaques, the chemoattractant factor modulating TREM2-dependent microglial responses has not been defined.
- Methods Potential binding of oligomeric amyloid-β 1-42 (oAβ 1-42 ) to TREM2 was tested by complementary approaches including solid phase binding, surface plasmon resonance and immunoprecipitation assays.
- The ability of oAβ 1-42 to activate TREM2 signaling pathways was examined by analyzing the phosphorylation of Syk and Akt in primary microglia as well as TREM2-mediated signaling in a reporter cell system.
Why it matters
This laboratory study tested whether small clumps of amyloid-beta (oligomeric Aβ 1-42) bind to TREM2, an immune sensor on the brain's microglia, using three separate binding methods, and whether this switches on TREM2 signalling (Syk and Akt) in microglia and in a reporter cell line; its title states that amyloid-beta "modulates microglial responses by binding to" TREM2. The background notes that TREM2 gene variants are linked to higher Alzheimer's risk and that the signal drawing microglia to plaques "has not been defined". It is cell and protein work with no people or treatment involved, so it does not show that changing this interaction affects Alzheimer's.
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Study details
- Evidence strengthLow
How this study scored 51/100
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 (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 | 2 / 5 | 2018 — 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 | 5 / 7 | Cited 220 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 22.0 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 3 / 6 | Cited 6.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 37 other studies in this library |
| Still being cited | 3 / 4 | Cited 64 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Xiao‐Fen Chen: h-index 29 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Mayo Clinic: institution h-index 1,606 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29587871) |
| Free to read | 2 / 2 | Free to read |
| Total | 51 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13024-018-0247-7
- PubMed: 29587871
- 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).
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. 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.
APA 7th
Zhong, L., Wang, Z., Wang, D., Martens, Y. A., Wu, L., Xu, Y., et al. (2018). Amyloid-beta modulates microglial responses by binding to the triggering receptor expressed on myeloid cells 2 (TREM2). Molecular neurodegeneration. https://doi.org/10.1186/s13024-018-0247-7
Vancouver
Zhong L, Wang Z, Wang D, Martens YA, Wu L, Xu Y, et al. Amyloid-beta modulates microglial responses by binding to the triggering receptor expressed on myeloid cells 2 (TREM2). Molecular neurodegeneration. 2018. doi:10.1186/s13024-018-0247-7. PMID: 29587871.
BibTeX
@article{zhong2018-29587871,
author = {Zhong, L. and Wang, Z. and Wang, D. and Martens, Y. A. and Wu, L. and Xu, Y. and Wang, K. and others},
title = {{Amyloid-beta modulates microglial responses by binding to the triggering receptor expressed on myeloid cells 2 (TREM2)}},
journal = {Molecular neurodegeneration},
year = {2018},
doi = {10.1186/s13024-018-0247-7},
pmid = {29587871},
url = {https://doi.org/10.1186/s13024-018-0247-7}
}
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