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Amyloid precursor protein processing and A beta42 deposition in a transgenic mouse model of Alzheimer disease
Johnson-Wood K, Lee M, Motter R, Hu K, Gordon G, Barbour R, Khan K, Gordon M et al.. Proceedings of the National Academy of Sciences of the United States of America, 1997-02-01
Topic: Brain proteins, microglia and lab models
The PDAPP transgenic mouse, which overexpresses human amyloid precursor protein (APP717V-->F), has been shown to develop much of the pathology associated with Alzheimer disease. In this report, levels of APP and its amyloidogenic metabolites were measured in brain regions of transgenic mice between 4 and 18 months of age. While absolute levels of APP expression likely contribute to the rate of amyloid beta-peptide (Abeta) deposition, regionally specific factors also seem important, as homozygotic mice express APP levels in pathologically unaffected regions in excess of that measured in certain amyloid plaque-prone regions of heterozygotic mice.
Key findings
- In this report, levels of APP and its amyloidogenic metabolites were measured in brain regions of transgenic mice between 4 and 18 months of age.
- While absolute levels of APP expression likely contribute to the rate of amyloid beta-peptide (Abeta) deposition, regionally specific factors also seem important, as homozygotic mice express APP levels in pathologically unaffected regions in excess of that measured in certain amyloid plaque-prone regions of heterozygotic mice.
- Regional levels of APP and APP-beta were nearly constant at all ages, while A beta levels dramatically and predictably increased in brain regions undergoing histochemically confirmed amyloidosis, most notably in the cortex and hippocampus.
- In hippocampus, A beta concentrations increase 17-fold between the ages of 4 and 8 months, and by 18 months of age are over 500-fold that at 4 months, reaching an average level in excess of 20 nmol of A beta per g of tissue.
Why it matters
In PDAPP mice engineered to overproduce a mutant human amyloid precursor protein (APP), this 1997 study measured APP and amyloid-beta (Aβ) in brain regions between 4 and 18 months of age. APP levels stayed 'nearly constant', while Aβ rose sharply where plaques formed: in the hippocampus it increased 17-fold from 4 to 8 months and over 500-fold by 18 months. Because some plaque-free regions made more APP than some plaque-prone ones, the authors suggest 'regionally specific factors also seem important'; this was a mouse study and tested no treatment.
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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 and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Proceedings of the National Academy of Sciences of the United States of America) |
| Journal's citation record | 4 / 4 | Proceedings of the National Academy of Sciences: journal h-index 1,167 (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 | 1997 — 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 | 6 / 7 | Cited 647 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 20.9 citations a year over 31 year(s) since 1997 |
| Impact for its field and year | 5 / 6 | Cited 21.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 39 other studies in this library |
| Still being cited | 2 / 4 | Cited 29 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Lisa McConlogue: h-index 36 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Elan Pharmaceuticals, Inc. (Ireland): institution h-index 241 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 9037091) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 48 / 100 | — |
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Read the original
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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.
APA 7th
Johnson-Wood, K., Lee, M., Motter, R., Hu, K., Gordon, G., Barbour, R., et al. (1997). Amyloid precursor protein processing and A beta42 deposition in a transgenic mouse model of Alzheimer disease. Proceedings of the National Academy of Sciences of the United States of America. https://doi.org/10.1073/pnas.94.4.1550
Vancouver
Johnson-Wood K, Lee M, Motter R, Hu K, Gordon G, Barbour R, et al. Amyloid precursor protein processing and A beta42 deposition in a transgenic mouse model of Alzheimer disease. Proceedings of the National Academy of Sciences of the United States of America. 1997. doi:10.1073/pnas.94.4.1550. PMID: 9037091.
BibTeX
@article{johnsonwood1997-9037091,
author = {Johnson-Wood, K. and Lee, M. and Motter, R. and Hu, K. and Gordon, G. and Barbour, R. and Khan, K. and Gordon, M. and others},
title = {{Amyloid precursor protein processing and A beta42 deposition in a transgenic mouse model of Alzheimer disease}},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
year = {1997},
doi = {10.1073/pnas.94.4.1550},
pmid = {9037091},
url = {https://doi.org/10.1073/pnas.94.4.1550}
}
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