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Uncovering Disease Mechanisms in a Novel Mouse Model Expressing Humanized APOEε4 and Trem2*R47H
Kotredes KP, Oblak A, Pandey RS, Lin PB, Garceau D, Williams H, Uyar A, O'Rourke R et al.. Frontiers in aging neuroscience, 2021-10-11
Topic: Brain proteins, microglia and lab models
Late-onset Alzheimer's disease (AD; LOAD) is the most common human neurodegenerative disease, however, the availability and efficacy of disease-modifying interventions is severely lacking. Despite exceptional efforts to understand disease progression via legacy amyloidogenic transgene mouse models, focus on disease translation with innovative mouse strains that better model the complexity of human AD is required to accelerate the development of future treatment modalities. LOAD within the human population is a polygenic and environmentally influenced disease with many risk factors acting in concert to produce disease processes parallel to those often muted by the early and aggressive aggregate formation in popular mouse strains.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Kotredes, K. P., Oblak, A., Pandey, R. S., Lin, P. B., Garceau, D., Williams, H., et al. (2021). Uncovering Disease Mechanisms in a Novel Mouse Model Expressing Humanized APOEε4 and Trem2*R47H. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2021.735524
Vancouver
Kotredes KP, Oblak A, Pandey RS, Lin PB, Garceau D, Williams H, et al. Uncovering Disease Mechanisms in a Novel Mouse Model Expressing Humanized APOEε4 and Trem2*R47H. Frontiers in aging neuroscience. 2021. doi:10.3389/fnagi.2021.735524. PMID: 34707490.
BibTeX
@article{kotredes2021-34707490,
author = {Kotredes, K. P. and Oblak, A. and Pandey, R. S. and Lin, P. B. and Garceau, D. and Williams, H. and Uyar, A. and O'Rourke, R. and others},
title = {{Uncovering Disease Mechanisms in a Novel Mouse Model Expressing Humanized APOEε4 and Trem2*R47H}},
journal = {Frontiers in aging neuroscience},
year = {2021},
doi = {10.3389/fnagi.2021.735524},
pmid = {34707490},
url = {https://doi.org/10.3389/fnagi.2021.735524}
}
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
- Despite exceptional efforts to understand disease progression via legacy amyloidogenic transgene mouse models, focus on disease translation with innovative mouse strains that better model the complexity of human AD is required to accelerate the development of future treatment modalities.
- LOAD within the human population is a polygenic and environmentally influenced disease with many risk factors acting in concert to produce disease processes parallel to those often muted by the early and aggressive aggregate formation in popular mouse strains.
- In addition to extracellular deposits of amyloid plaques and inclusions of the microtubule-associated protein tau, AD is also defined by synaptic/neuronal loss, vascular deficits, and neuroinflammation.
- These underlying processes need to be better defined, how the disease progresses with age, and compared to human-relevant outcomes.
Why it matters
This paper describes a new mouse model expressing humanized APOEε4 and Trem2*R47H to better model late-onset Alzheimer's disease. It is animal model development, so it is early and does not yet show a treatment for people.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Study designcross-sectional
- Evidence strengthLow
How this study scored 50/100
Published in a peer-reviewed journal, and it is a snapshot of people at one point in time. Scored zero for 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 (Frontiers in aging neuroscience) |
| Journal's citation record | 2 / 4 | Frontiers in Aging Neuroscience: journal h-index 174 (OpenAlex, 2026-10-29) |
| Study design | 4 / 12 | A snapshot of people at one point in time |
| 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 | 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 | 4 / 7 | Cited 66 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 9.4 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 | 2 / 4 | Cited 30 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Gareth R. Howell: h-index 50 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Pittsburgh: institution h-index 1,470 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 34707490) |
| Free to read | 2 / 2 | Free to read |
| Total | 50 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3389/fnagi.2021.735524
- PubMed: 34707490
- Original source →
- Free full text: Frontiers in Aging Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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