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Knock-in models related to Alzheimer's disease: synaptic transmission, plaques and the role of microglia
Benitez DP, Jiang S, Wood J, Wang R, Hall CM, Peerboom C, Wong N, Stringer KM et al.. Molecular neurodegeneration, 2021-07-15
Topic: Amyloid, tau and blood-test diagnosis
Background Microglia are active modulators of Alzheimer's disease but their role in relation to amyloid plaques and synaptic changes due to rising amyloid beta is unclear. We add novel findings concerning these relationships and investigate which of our previously reported results from transgenic mice can be validated in knock-in mice, in which overexpression and other artefacts of transgenic technology are avoided. Methods App NL-F and App NL-G-F knock-in mice expressing humanised amyloid beta with mutations in App that cause familial Alzheimer's disease were compared to wild type mice throughout life.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Benitez, D. P., Jiang, S., Wood, J., Wang, R., Hall, C. M., Peerboom, C., et al. (2021). Knock-in models related to Alzheimer's disease: synaptic transmission, plaques and the role of microglia. Molecular neurodegeneration. https://doi.org/10.1186/s13024-021-00457-0
Vancouver
Benitez DP, Jiang S, Wood J, Wang R, Hall CM, Peerboom C, et al. Knock-in models related to Alzheimer's disease: synaptic transmission, plaques and the role of microglia. Molecular neurodegeneration. 2021. doi:10.1186/s13024-021-00457-0. PMID: 34266459.
BibTeX
@article{benitez2021-34266459,
author = {Benitez, D. P. and Jiang, S. and Wood, J. and Wang, R. and Hall, C. M. and Peerboom, C. and Wong, N. and Stringer, K. M. and others},
title = {{Knock-in models related to Alzheimer's disease: synaptic transmission, plaques and the role of microglia}},
journal = {Molecular neurodegeneration},
year = {2021},
doi = {10.1186/s13024-021-00457-0},
pmid = {34266459},
url = {https://doi.org/10.1186/s13024-021-00457-0}
}
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
- We add novel findings concerning these relationships and investigate which of our previously reported results from transgenic mice can be validated in knock-in mice, in which overexpression and other artefacts of transgenic technology are avoided.
- Methods App NL-F and App NL-G-F knock-in mice expressing humanised amyloid beta with mutations in App that cause familial Alzheimer's disease were compared to wild type mice throughout life.
- In vitro approaches were used to understand microglial alterations at the genetic and protein levels and synaptic function and plasticity in CA1 hippocampal neurones, each in relationship to both age and stage of amyloid beta pathology.
- The contribution of microglia to neuronal function was further investigated by ablating microglia with CSF1R inhibitor PLX5622.
Why it matters
This study used knock-in mice expressing humanised amyloid beta with familial Alzheimer's disease mutations to examine synaptic transmission, plaques, and microglial roles. It is animal research and does not report a treatment, cure, or prevention for Alzheimer's disease in people.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 48/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / 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 | 3 / 5 | 2021 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 79 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 11.3 citations a year over 7 year(s) since 2021 |
| Impact for its field and year | 3 / 6 | Cited 6.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 3 / 4 | Cited 55 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Damian M. Cummings: h-index 26 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University College London: institution h-index 2,029 (OpenAlex) |
| Multicenter collaboration | 3 / 3 | OpenAlex lists 13 institution(s) in 7 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 34266459) |
| Free to read | 2 / 2 | Free to read |
| Total | 48 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13024-021-00457-0
- PubMed: 34266459
- 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).
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