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TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration
Xie M, Liu YU, Zhao S, Zhang L, Bosco DB, Pang YP, Zhong J, Sheth U et al.. Nature neuroscience, 2021-12-16
Topic: Brain proteins, microglia and lab models
Triggering receptor expressed on myeloid cell 2 (TREM2) is linked to risk of neurodegenerative disease. However, the function of TREM2 in neurodegeneration is still not fully understood. Here, we investigated the role of microglial TREM2 in TAR DNA-binding protein 43 (TDP-43)-related neurodegeneration using virus-mediated and transgenic mouse models.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Xie, M., Liu, Y. U., Zhao, S., Zhang, L., Bosco, D. B., Pang, Y. P., et al. (2022). TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration. Nature neuroscience. https://doi.org/10.1038/s41593-021-00975-6
Vancouver
Xie M, Liu YU, Zhao S, Zhang L, Bosco DB, Pang YP, et al. TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration. Nature neuroscience. 2022. doi:10.1038/s41593-021-00975-6. PMID: 34916658.
BibTeX
@article{xie2022-34916658,
author = {Xie, M. and Liu, Y. U. and Zhao, S. and Zhang, L. and Bosco, D. B. and Pang, Y. P. and Zhong, J. and Sheth, U. and others},
title = {{TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration}},
journal = {Nature neuroscience},
year = {2022},
doi = {10.1038/s41593-021-00975-6},
pmid = {34916658},
url = {https://doi.org/10.1038/s41593-021-00975-6}
}
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
- However, the function of TREM2 in neurodegeneration is still not fully understood.
- Here, we investigated the role of microglial TREM2 in TAR DNA-binding protein 43 (TDP-43)-related neurodegeneration using virus-mediated and transgenic mouse models.
- We found that TREM2 deficiency impaired phagocytic clearance of pathological TDP-43 by microglia and enhanced neuronal damage and motor impairments.
- Mass cytometry analysis revealed that human TDP-43 (hTDP-43) induced a TREM2-dependent subpopulation of microglia with high CD11c expression and phagocytic ability.
Why it matters
In mice, losing TREM2 reduced microglia's ability to clear abnormal TDP-43 protein and worsened nerve cell damage and movement problems. This is early animal work on TDP-43-related neurodegeneration, not a treatment or cure for Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 55/100
Published in a leading specialty 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 | 9 / 10 | Tier 2 — leading specialty journal (Nature neuroscience) |
| Journal's citation record | 4 / 4 | Nature Neuroscience: journal h-index 593 (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 | 3 / 5 | 2022 — within 6 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 157 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 26.2 citations a year over 6 year(s) since 2022 |
| Impact for its field and year | 3 / 6 | Cited 7.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 7 other studies in this library |
| Still being cited | 3 / 4 | Cited 113 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Long‐Jun Wu: h-index 76 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Johns Hopkins University: institution h-index 2,306 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 34916658) |
| Free to read | 2 / 2 | Free to read |
| Total | 55 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1038/s41593-021-00975-6
- PubMed: 34916658
- Original source →
- Free full text: bioRxiv (Cold Spring Harbor Laboratory) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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