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Cited by 1,431Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease

Janus, Christopher, Pearson, Jacqueline, McLaurin, JoAnne, Mathews, Paul M., Jiang, Ying, Schmidt, Stephen D., Chishti, M. Azhar, Horne, Patrick, Heslin, Donna, French, Janet, Mount, Howard T.J., Nixon, Ralph A., Mercken, Marc, Bergeron, Catherine, Fraser, Paul E., St George-Hyslop, Peter, Westaway, David·2000·Nature
DOI 10.1038/35050110
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Abstract

Much evidence indicates that abnormal processing and extracellular deposition of amyloid-beta peptide (A beta), a proteolytic derivative of the beta-amyloid precursor protein (betaAPP), is central to the pathogenesis of Alzheimer's disease (reviewed in ref. 1). In the PDAPP transgenic mouse model of Alzheimer's disease, immunization with A beta causes a marked reduction in burden of the brain amyloid. Evidence that A beta immunization also reduces cognitive dysfunction in murine models of Alzheimer's disease would support the hypothesis that abnormal A beta processing is essential to the pathogenesis of Alzheimer's disease, and would encourage the development of other strategies directed at the 'amyloid cascade'. Here we show that A beta immunization reduces both deposition of cerebral fibrillar A beta and cognitive dysfunction in the TgCRND8 murine model of Alzheimer's disease without, however, altering total levels of A beta in the brain. This implies that either a approximately 50% reduction in dense-cored A beta plaques is sufficient to affect cognition, or that vaccination may modulate the activity/abundance of a small subpopulation of especially toxic A beta species.

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Research works printed but not linked: 24

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Metadata

Authors
Janus, C., Pearson, J., McLaurin, J., Mathews, P. M., Jiang, Y., Schmidt, S. D., Chishti, M. A., Horne, P., Heslin, D., French, J., Mount, H. T. J., Nixon, R. A., Mercken, M., Bergeron, C., Fraser, P. E., St George-Hyslop, P., & Westaway, D.
Affiliations
  • University of Toronto (CA)
  • New York University (US)
  • Janssen (Belgium) (BE)
  • University Health Network (CA)
ORCID
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
2000-12
Volume
408
Issue
6815
Pages
979-982
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
DOI
10.1038/35050110
OpenAlex
W1965275873
Cited by
1,431
References
6
Citations by year
2026: 7 · 2025: 11 · 2024: 16 · 2023: 22 · 2022: 21 · 2021: 15 · 2020: 26 · 2019: 26 · 2018: 25 · 2017: 31 · 2016: 30 · 2015: 35 · 2014: 46 · 2013: 59 · 2012: 61
FWCI
69.52
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
Funders
Medical Research Council
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
amyloid-beta immunization, Alzheimer's disease, amyloid plaques, cognitive impairment, TgCRND8 mice, amyloid hypothesis, amyloid-beta processing, amyloid precursor protein
MeSH terms
Alzheimer Disease, Amyloid, Animals, Disease Models, Animal, Cricetinae, Hippocampus, Humans, Mesocricetus, Mice, Inbred C3H, Mice, Transgenic, Peptide Fragments, Vaccination, Amyloid beta-Peptides, Maze Learning, Mice, Plaque, Amyloid, Islet Amyloid Polypeptide

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