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Absence of microglia promotes diverse pathologies and early lethality in Alzheimer's disease mice
Kiani Shabestari S, Morabito S, Danhash EP, McQuade A, Sanchez JR, Miyoshi E, Chadarevian JP, Claes C et al.. Cell reports, 2022-06-01
Topic: Amyloid, tau and blood-test diagnosis
Microglia are strongly implicated in the development and progression of Alzheimer's disease (AD), yet their impact on pathology and lifespan remains unclear. Here we utilize a CSF1R hypomorphic mouse to generate a model of AD that genetically lacks microglia. The resulting microglial-deficient mice exhibit a profound shift from parenchymal amyloid plaques to cerebral amyloid angiopathy (CAA), which is accompanied by numerous transcriptional changes, greatly increased brain calcification and hemorrhages, and premature lethality.
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APA 7th
Kiani Shabestari, S., Morabito, S., Danhash, E. P., McQuade, A., Sanchez, JR., Miyoshi, E., et al. (2022). Absence of microglia promotes diverse pathologies and early lethality in Alzheimer's disease mice. Cell reports. https://doi.org/10.1016/j.celrep.2022.110961
Vancouver
Kiani Shabestari S, Morabito S, Danhash EP, McQuade A, Sanchez JR, Miyoshi E, et al. Absence of microglia promotes diverse pathologies and early lethality in Alzheimer's disease mice. Cell reports. 2022. doi:10.1016/j.celrep.2022.110961. PMID: 35705056.
BibTeX
@article{kianishabestari2022-35705056,
author = {Kiani Shabestari, S. and Morabito, S. and Danhash, E. P. and McQuade, A. and Sanchez, JR. and Miyoshi, E. and Chadarevian, J. P. and Claes, C. and others},
title = {{Absence of microglia promotes diverse pathologies and early lethality in Alzheimer's disease mice}},
journal = {Cell reports},
year = {2022},
doi = {10.1016/j.celrep.2022.110961},
pmid = {35705056},
url = {https://doi.org/10.1016/j.celrep.2022.110961}
}
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Key findings
- Here we utilize a CSF1R hypomorphic mouse to generate a model of AD that genetically lacks microglia.
- The resulting microglial-deficient mice exhibit a profound shift from parenchymal amyloid plaques to cerebral amyloid angiopathy (CAA), which is accompanied by numerous transcriptional changes, greatly increased brain calcification and hemorrhages, and premature lethality.
- Remarkably, a single injection of wild-type microglia into adult mice repopulates the microglial niche and prevents each of these pathological changes.
- Taken together, these results indicate the protective functions of microglia in reducing CAA, blood-brain barrier dysfunction, and brain calcification.
Why it matters
In mice engineered to lack microglia, amyloid plaques shifted to cerebral amyloid angiopathy with bleeding, calcification and early death, and injecting normal microglia prevented these problems. These are mouse results and do not establish a treatment, cure or prevention for people.
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Study details
- Evidence strengthLow
How this study scored 53/100
Published in a peer-reviewed 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 | 7 / 10 | Tier 3 — peer-reviewed journal (Cell reports) |
| Journal's citation record | 3 / 4 | Cell Reports: journal h-index 321 (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 | Laboratory or animal study (title names “mice”) — 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 169 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 28.2 citations a year over 6 year(s) since 2022 |
| Impact for its field and year | 4 / 6 | Cited 10.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 3 / 4 | Cited 120 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Mathew M. Blurton-Jones: h-index 57 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | The University of Queensland: institution h-index 1,516 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 35705056) |
| Free to read | 2 / 2 | Free to read |
| Total | 53 / 100 | — |
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