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Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease
Bard F, Cannon C, Barbour R, Burke RL, Games D, Grajeda H, Guido T, Hu K et al.. Nature medicine, 2000-08-01
Topic: Brain proteins, microglia and lab models
One hallmark of Alzheimer disease is the accumulation of amyloid beta-peptide in the brain and its deposition as plaques. Mice transgenic for an amyloid beta precursor protein (APP) mini-gene driven by a platelet-derived (PD) growth factor promoter (PDAPP mice), which overexpress one of the disease-linked mutant forms of the human amyloid precursor protein, show many of the pathological features of Alzheimer disease, including extensive deposition of extracellular amyloid plaques, astrocytosis and neuritic dystrophy. Active immunization of PDAPP mice with human amyloid beta-peptide reduces plaque burden and its associated pathologies.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Bard, F., Cannon, C., Barbour, R., Burke, R. L., Games, D., Grajeda, H., et al. (2000). Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease. Nature medicine. https://doi.org/10.1038/78682
Vancouver
Bard F, Cannon C, Barbour R, Burke RL, Games D, Grajeda H, et al. Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease. Nature medicine. 2000. doi:10.1038/78682. PMID: 10932230.
BibTeX
@article{bard2000-10932230,
author = {Bard, F. and Cannon, C. and Barbour, R. and Burke, R. L. and Games, D. and Grajeda, H. and Guido, T. and Hu, K. and others},
title = {{Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease}},
journal = {Nature medicine},
year = {2000},
doi = {10.1038/78682},
pmid = {10932230},
url = {https://doi.org/10.1038/78682}
}
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
- Mice transgenic for an amyloid beta precursor protein (APP) mini-gene driven by a platelet-derived (PD) growth factor promoter (PDAPP mice), which overexpress one of the disease-linked mutant forms of the human amyloid precursor protein, show many of the pathological features of Alzheimer disease, including extensive deposition of extracellular amyloid plaques, astrocytosis and neuritic dystrophy.
- Active immunization of PDAPP mice with human amyloid beta-peptide reduces plaque burden and its associated pathologies.
- Several hypotheses have been proposed regarding the mechanism of this response.
- Here we report that peripheral administration of antibodies against amyloid beta-peptide, was sufficient to reduce amyloid burden.
Why it matters
Earlier work had shown that immunizing PDAPP mice with human amyloid-beta "reduces plaque burden and its associated pathologies". This 2000 study reports that giving antibodies against amyloid-beta from outside the brain "was sufficient to reduce amyloid burden", and its title says the antibodies entered the central nervous system. Our record gives no effect sizes, memory or safety data, and these were genetically engineered mice, so it does not show that the approach works or is safe in people.
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Study details
- Evidence strengthLow
How this study scored 55/100
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 medicine) |
| Journal's citation record | 4 / 4 | Nature Medicine: journal h-index 763 (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 | 2000 — 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 2,021 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 72.2 citations a year over 28 year(s) since 2000 |
| Impact for its field and year | 6 / 6 | Cited 63.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 78 other studies in this library |
| Still being cited | 3 / 4 | Cited 99 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Ted A. Yednock: h-index 45 (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 10932230) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 55 / 100 | — |
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Also tagged “amyloid-beta”
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