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Alzheimer's disease modification mediated by bone marrow-derived macrophages via a TREM2-independent pathway in mouse model of amyloidosis
Dvir-Szternfeld R, Castellani G, Arad M, Cahalon L, Colaiuta SP, Keren-Shaul H, Croese T, Burgaletto C et al.. Nature aging, 2021-12-20
Topic: Brain proteins, microglia and lab models
Microglia and monocyte-derived macrophages (MDM) are key players in dealing with Alzheimer's disease. In amyloidosis mouse models, activation of microglia was found to be TREM2 dependent. Here, using Trem2 -/- 5xFAD mice, we assessed whether MDM act via a TREM2-dependent pathway. We adopted a treatment protocol targeting the programmed cell death ligand-1 (PD-L1) immune checkpoint, previously shown to modify Alzheimer's disease via MDM involvement. Blockade of PD-L1 in Trem2 -/- 5xFAD mice resulted in cognitive improvement and reduced levels of water-soluble amyloid beta 1-42 with no effect on amyloid plaque burden. Single-cell RNA sequencing revealed that MDM, derived from both Trem2 -/- and Trem2 +/+ 5xFAD mouse brains, express a unique set of genes encoding scavenger receptors (for example, Mrc1, Msr1). Blockade of monocyte trafficking using anti-CCR2 antibody completely abrogated the cognitive improvement induced by anti-PD-L1 treatment in Trem2 -/- 5xFAD mice and similarly, but to a lesser extent, in Trem2 +/+ 5xFAD mice. These results highlight a TREM2-independent, disease-modifying activity of MDM in an amyloidosis mouse model.
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APA 7th
Dvir-Szternfeld, R., Castellani, G., Arad, M., Cahalon, L., Colaiuta, S. P., Keren-Shaul, H., et al. (2022). Alzheimer's disease modification mediated by bone marrow-derived macrophages via a TREM2-independent pathway in mouse model of amyloidosis. Nature aging. https://doi.org/10.1038/s43587-021-00149-w
Vancouver
Dvir-Szternfeld R, Castellani G, Arad M, Cahalon L, Colaiuta SP, Keren-Shaul H, et al. Alzheimer's disease modification mediated by bone marrow-derived macrophages via a TREM2-independent pathway in mouse model of amyloidosis. Nature aging. 2022. doi:10.1038/s43587-021-00149-w. PMID: 37118355.
BibTeX
@article{dvirszternfeld2022-37118355,
author = {Dvir-Szternfeld, R. and Castellani, G. and Arad, M. and Cahalon, L. and Colaiuta, S. P. and Keren-Shaul, H. and Croese, T. and Burgaletto, C. and others},
title = {{Alzheimer's disease modification mediated by bone marrow-derived macrophages via a TREM2-independent pathway in mouse model of amyloidosis}},
journal = {Nature aging},
year = {2022},
doi = {10.1038/s43587-021-00149-w},
pmid = {37118355},
url = {https://doi.org/10.1038/s43587-021-00149-w}
}
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Key findings
- Single-cell RNA sequencing revealed that MDM, derived from both Trem2 -/- and Trem2 +/+ 5xFAD mouse brains, express a unique set of genes encoding scavenger receptors (for example, Mrc1, Msr1).
- These results highlight a TREM2-independent, disease-modifying activity of MDM in an amyloidosis mouse model.
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Study details
- Evidence strengthLow
How this study scored 43/100
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. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 25 of the 58 points we could judge it on, which is 43 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Nature aging) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 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 | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 37118355) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 25 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 25 of the 58 points we could judge it on is 43 out of 100. |
| Total | 43 / 100 | — |
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