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Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Karen Hsiao, Paul F. Chapman, Steven P. Nilsen, Chris Eckman, Yasuo Harigaya, Steven G. Younkin, Fusheng Yang, Greg M. Cole. Science, 1996-10-04
Topic: Brain proteins, microglia and lab models
Transgenic mice overexpressing the 695-amino acid isoform of human Alzheimer beta-amyloid (Abeta) precursor protein containing a Lys670 --> Asn, Met671 --> Leu mutation had normal learning and memory in spatial reference and alternation tasks at 3 months of age but showed impairment by 9 to 10 months of age. A fivefold increase in Abeta(1-40) and a 14-fold increase in Abeta(1-42/43) accompanied the appearance of these behavioral deficits. Numerous Abeta plaques that stained with Congo red dye were present in cortical and limbic structures of mice with elevated amounts of Abeta. The correlative appearance of behavioral, biochemical, and pathological abnormalities reminiscent of Alzheimer's disease in these transgenic mice suggests new opportunities for exploring the pathophysiology and neurobiology of this disease.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Hsiao, K., Chapman, P. F., Nilsen, S. P., Eckman, C., Harigaya, Y., Younkin, S. G., et al. (1996). Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice. Science. https://doi.org/10.1126/science.274.5284.99
Vancouver
Hsiao K, Chapman PF, Nilsen SP, Eckman C, Harigaya Y, Younkin SG, et al. Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice. Science. 1996. doi:10.1126/science.274.5284.99. PMID: 8810256.
BibTeX
@article{hsiao1996-8810256,
author = {Hsiao, Karen and Chapman, Paul F. and Nilsen, Steven P. and Eckman, Chris and Harigaya, Yasuo and Younkin, Steven G. and Yang, Fusheng and Cole, Greg M.},
title = {{Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice}},
journal = {Science},
year = {1996},
doi = {10.1126/science.274.5284.99},
pmid = {8810256},
url = {https://doi.org/10.1126/science.274.5284.99}
}
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 names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Transgenic mice overexpressing the 695-amino acid isoform of human Alzheimer beta-amyloid (Abeta) precursor protein containing a Lys670 --> Asn, Met671 --> Leu mutation had normal learning and memory in spatial reference and alternation tasks at 3 months of age but showed impairment by 9 to 10 months of age.
- A fivefold increase in Abeta(1-40) and a 14-fold increase in Abeta(1-42/43) accompanied the appearance of these behavioral deficits.
- Numerous Abeta plaques that stained with Congo red dye were present in cortical and limbic structures of mice with elevated amounts of Abeta.
- The correlative appearance of behavioral, biochemical, and pathological abnormalities reminiscent of Alzheimer's disease in these transgenic mice suggests new opportunities for exploring the pathophysiology and neurobiology of this disease.
Why it matters
This study in transgenic mice found that mice overexpressing a mutant form of human amyloid precursor protein showed normal learning and memory at 3 months but impairment by 9 to 10 months, accompanied by elevated Aβ and amyloid plaques. It is an animal study and does not directly address treating, curing, or preventing Alzheimer's disease in humans.
Study details
- Evidence strengthLow
How this study scored 62/100
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 (Science) |
| Journal's citation record | 4 / 4 | Science: journal h-index 1,754 (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 | 1996 — 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 4,220 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 131.9 citations a year over 32 year(s) since 1996 |
| Impact for its field and year | 6 / 6 | Cited 68.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 5 / 6 | Cited by 128 other studies in this library |
| Still being cited | 4 / 4 | Cited 212 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Greg M. Cole: h-index 60 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California, Los Angeles: institution h-index 1,923 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 8810256) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 62 / 100 | — |
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