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Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease
Garcia-Alloza M, Robbins EM, Zhang-Nunes SX, Purcell SM, Betensky RA, Raju S, Prada C, Greenberg SM et al.. Neurobiology of disease, 2006-10-05
Topic: Amyloid, tau and blood-test diagnosis
Transgenic mice carrying disease-linked forms of genes associated with Alzheimer disease often demonstrate deposition of the beta-amyloid as senile plaques and cerebral amyloid angiopathy. We have characterized the natural history of beta-amyloid deposition in APPswe/PS1dE9 mice, a particularly aggressive transgenic mouse model generated with mutant transgenes for APP (APPswe: KM594/5NL) and PS1 (dE9: deletion of exon 9). Ex vivo histochemistry showed Abeta deposition by 4 months with a progressive increase in plaque number up to 12 months and a similar increase of Abeta levels.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Garcia-Alloza, M., Robbins, E. M., Zhang-Nunes, S. X., Purcell, S. M., Betensky, R. A., Raju, S., et al. (2006). Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease. Neurobiology of disease. https://doi.org/10.1016/j.nbd.2006.08.017
Vancouver
Garcia-Alloza M, Robbins EM, Zhang-Nunes SX, Purcell SM, Betensky RA, Raju S, et al. Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease. Neurobiology of disease. 2006. doi:10.1016/j.nbd.2006.08.017. PMID: 17029828.
BibTeX
@article{garciaalloza2006-17029828,
author = {Garcia-Alloza, M. and Robbins, E. M. and Zhang-Nunes, S. X. and Purcell, S. M. and Betensky, R. A. and Raju, S. and Prada, C. and Greenberg, S. M. and others},
title = {{Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease}},
journal = {Neurobiology of disease},
year = {2006},
doi = {10.1016/j.nbd.2006.08.017},
pmid = {17029828},
url = {https://doi.org/10.1016/j.nbd.2006.08.017}
}
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 have characterized the natural history of beta-amyloid deposition in APPswe/PS1dE9 mice, a particularly aggressive transgenic mouse model generated with mutant transgenes for APP (APPswe: KM594/5NL) and PS1 (dE9: deletion of exon 9).
- Ex vivo histochemistry showed Abeta deposition by 4 months with a progressive increase in plaque number up to 12 months and a similar increase of Abeta levels.
- In vivo multiphoton microscopy at weekly intervals showed increasing beta-amyloid deposition as CAA and plaques.
- Although first appearing at an early age, CAA progressed at a significantly slower rate than in the Tg2576 mice.
Why it matters
This study characterized the natural history of amyloid-beta deposition in APPswe/PS1dE9 transgenic mice, showing deposition by 4 months with progressive increases in plaque number and amyloid-beta levels up to 12 months. It is an animal model study and reports no treatment, cure or prevention in humans.
Study details
- Evidence strengthLow
How this study scored 51/100
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 (Neurobiology of disease) |
| Journal's citation record | 2 / 4 | Neurobiology of Disease: journal h-index 225 (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 | 2006 — 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 “mouse”) — 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 749 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 34.0 citations a year over 22 year(s) since 2006 |
| Impact for its field and year | 4 / 6 | Cited 9.2× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 19 other studies in this library |
| Still being cited | 3 / 4 | Cited 107 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Matthew P. Frosch: h-index 120 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 17029828) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 51 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.nbd.2006.08.017
- PubMed: 17029828
- Original source →
- Free full text: DOAJ (DOAJ: Directory of Open Access Journals) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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