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Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse
Schenk D, Barbour R, Dunn W, Gordon G, Grajeda H, Guido T, Hu K, Huang J et al.. Nature, 1999-07-01
Topic: Amyloid, tau and blood-test diagnosis
Amyloid-beta peptide (Abeta) seems to have a central role in the neuropathology of Alzheimer's disease (AD). Familial forms of the disease have been linked to mutations in the amyloid precursor protein (APP) and the presenilin genes. Disease-linked mutations in these genes result in increased production of the 42-amino-acid form of the peptide (Abeta42), which is the predominant form found in the amyloid plaques of Alzheimer's disease.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Schenk, D., Barbour, R., Dunn, W., Gordon, G., Grajeda, H., Guido, T., et al. (1999). Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature. https://doi.org/10.1038/22124
Vancouver
Schenk D, Barbour R, Dunn W, Gordon G, Grajeda H, Guido T, et al. Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature. 1999. doi:10.1038/22124. PMID: 10408445.
BibTeX
@article{schenk1999-10408445,
author = {Schenk, D. and Barbour, R. and Dunn, W. and Gordon, G. and Grajeda, H. and Guido, T. and Hu, K. and Huang, J. and others},
title = {{Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse}},
journal = {Nature},
year = {1999},
doi = {10.1038/22124},
pmid = {10408445},
url = {https://doi.org/10.1038/22124}
}
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
- Familial forms of the disease have been linked to mutations in the amyloid precursor protein (APP) and the presenilin genes.
- Disease-linked mutations in these genes result in increased production of the 42-amino-acid form of the peptide (Abeta42), which is the predominant form found in the amyloid plaques of Alzheimer's disease.
- The PDAPP transgenic mouse, which overexpresses mutant human APP (in which the amino acid at position 717 is phenylalanine instead of the normal valine), progressively develops many of the neuropathological hallmarks of Alzheimer's disease in an age- and brain-region-dependent manner.
- In the present study, transgenic animals were immunized with Abeta42, either before the onset of AD-type neuropathologies (at 6 weeks of age) or at an older age (11 months), when amyloid-beta deposition and several of the subsequent neuropathological changes were well established.
Why it matters
In this 1999 Nature study, PDAPP mice — engineered to carry a mutant human APP gene and to develop "many of the neuropathological hallmarks of Alzheimer's disease" — were immunized with the Abeta42 peptide either at 6 weeks of age, before pathology began, or at 11 months, when it was "well established". The study reports that immunization "attenuates Alzheimer-disease-like pathology"; our record does not include how large the effect was, which changes were measured, or any effect on memory. These were mice only, so the result says nothing directly about whether this works, or is safe, in people.
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Study details
- Evidence strengthLow
How this study scored 57/100
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 | 1999 — 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 | 7 / 7 | Cited 3,173 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 109.4 citations a year over 29 year(s) since 1999 |
| Impact for its field and year | 6 / 6 | Cited 94.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 5 / 6 | Cited by 114 other studies in this library |
| Still being cited | 3 / 4 | Cited 136 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Peter A. Seubert: h-index 60 (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 10408445) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 57 / 100 | — |
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