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

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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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Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse
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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: Janus, Christopher
McLaurin, JoAnne
Mathews, Paul M.
Mount, Howard T.J.
Nixon, Ralph A.
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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Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease

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