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Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein
Games D, Adams D, Alessandrini R, Barbour R, Berthelette P, Blackwell C, Carr T, Clemens J et al.. Nature, 1995-02-01
Topic: Brain proteins, microglia and lab models
Alzheimer's disease (AD) is the most common cause of progressive intellectual failure in aged humans. AD brains contain numerous amyloid plaques surrounded by dystrophic neurites, and show profound synaptic loss, neurofibrillary tangle formation and gliosis. The amyloid plaques are composed of amyloid beta-peptide (A beta), a 40-42-amino-acid fragment of the beta-amyloid precursor protein (APP).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Games, D., Adams, D., Alessandrini, R., Barbour, R., Berthelette, P., Blackwell, C., et al. (1995). Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein. Nature. https://doi.org/10.1038/373523a0
Vancouver
Games D, Adams D, Alessandrini R, Barbour R, Berthelette P, Blackwell C, et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein. Nature. 1995. doi:10.1038/373523a0. PMID: 7845465.
BibTeX
@article{games1995-7845465,
author = {Games, D. and Adams, D. and Alessandrini, R. and Barbour, R. and Berthelette, P. and Blackwell, C. and Carr, T. and Clemens, J. and others},
title = {{Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein}},
journal = {Nature},
year = {1995},
doi = {10.1038/373523a0},
pmid = {7845465},
url = {https://doi.org/10.1038/373523a0}
}
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
- AD brains contain numerous amyloid plaques surrounded by dystrophic neurites, and show profound synaptic loss, neurofibrillary tangle formation and gliosis.
- The amyloid plaques are composed of amyloid beta-peptide (A beta), a 40-42-amino-acid fragment of the beta-amyloid precursor protein (APP).
- A primary pathogenic role for APP/A beta is suggested by missense mutations in APP that are tightly linked to autosomal dominant forms of AD.
- A major obstacle to elucidating and treating AD has been the lack of an animal model.
Why it matters
This 1995 Nature paper describes transgenic mice that overexpress a mutant (V717F) form of the amyloid precursor protein, which its title says show "Alzheimer-type neuropathology". It was motivated by APP mutations "tightly linked to autosomal dominant forms of AD" and by "the lack of an animal model"; our record does not say which brain changes the mice developed, at what age, or whether memory was affected. These are mice, not people, so the study does not show how to treat or prevent Alzheimer's in humans.
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Study details
- Evidence strengthLow
How this study scored 59/100
Published in a top-tier 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 | 10 / 10 | Tier 1 — top-tier general journal (Nature) |
| Journal's citation record | 4 / 4 | Nature: journal h-index 1,841 (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 | 1 / 5 | 1995 — older than 20 years, still counted |
| 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 “transgenic”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 7 / 7 | Cited 2,523 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 76.5 citations a year over 33 year(s) since 1995 |
| Impact for its field and year | 6 / 6 | Cited 97.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 92 other studies in this library |
| Still being cited | 3 / 4 | Cited 106 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Jun Wei Zhao: h-index 30 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California San Diego: institution h-index 1,852 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 9 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 7845465) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 59 / 100 | — |
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