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Identification of senescent, TREM2-expressing microglia in aging and Alzheimer's disease model mouse brain
Rachmian N, Medina S, Cherqui U, Akiva H, Deitch D, Edilbi D, Croese T, Salame TM et al.. Nature neuroscience, 2024-04-18
Topic: Brain proteins, microglia and lab models
Alzheimer's disease (AD) and dementia in general are age-related diseases with multiple contributing factors, including brain inflammation. Microglia, and specifically those expressing the AD risk gene TREM2, are considered important players in AD, but their exact contribution to pathology remains unclear. In this study, using high-throughput mass cytometry in the 5×FAD mouse model of amyloidosis, we identified senescent microglia that express high levels of TREM2 but also exhibit a distinct signature from TREM2-dependent disease-associated microglia (DAM).
Key findings
- Microglia, and specifically those expressing the AD risk gene TREM2, are considered important players in AD, but their exact contribution to pathology remains unclear.
- In this study, using high-throughput mass cytometry in the 5×FAD mouse model of amyloidosis, we identified senescent microglia that express high levels of TREM2 but also exhibit a distinct signature from TREM2-dependent disease-associated microglia (DAM).
- This senescent microglial protein signature was found in various mouse models that show cognitive decline, including aging, amyloidosis and tauopathy.
- TREM2-null mice had fewer microglia with a senescent signature.
Why it matters
Using high-throughput mass cytometry in mice, this study identified senescent microglia (the brain's immune cells) that carry high levels of the Alzheimer's risk gene TREM2 but are distinct from the better-known "disease-associated microglia." The same protein signature appeared in old mice and in mouse models of amyloid and tau build-up that show cognitive decline, and mice lacking TREM2 had fewer of these cells. This is mouse-only research that links TREM2 to an aging-like microglial state; it does not show cause in people or test any treatment.
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Study details
- Evidence strengthLow
How this study scored 54/100
Published in a leading specialty 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 | 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 | 4 / 5 | 2024 — within 3 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 “mouse”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 182 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 45.5 citations a year over 4 year(s) since 2024 |
| Impact for its field and year | 5 / 6 | Cited 24.8× 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 182 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Michal Schwartz: h-index 105 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Weizmann Institute of Science: institution h-index 1,080 (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 38637622) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 54 / 100 | — |
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Read the original
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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
Rachmian, N., Medina, S., Cherqui, U., Akiva, H., Deitch, D., Edilbi, D., et al. (2024). Identification of senescent, TREM2-expressing microglia in aging and Alzheimer's disease model mouse brain. Nature neuroscience. https://doi.org/10.1038/s41593-024-01620-8
Vancouver
Rachmian N, Medina S, Cherqui U, Akiva H, Deitch D, Edilbi D, et al. Identification of senescent, TREM2-expressing microglia in aging and Alzheimer's disease model mouse brain. Nature neuroscience. 2024. doi:10.1038/s41593-024-01620-8. PMID: 38637622.
BibTeX
@article{rachmian2024-38637622,
author = {Rachmian, N. and Medina, S. and Cherqui, U. and Akiva, H. and Deitch, D. and Edilbi, D. and Croese, T. and Salame, T. M. and others},
title = {{Identification of senescent, TREM2-expressing microglia in aging and Alzheimer's disease model mouse brain}},
journal = {Nature neuroscience},
year = {2024},
doi = {10.1038/s41593-024-01620-8},
pmid = {38637622},
url = {https://doi.org/10.1038/s41593-024-01620-8}
}
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