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

Christopher Janus, Jacqueline Pearson, JoAnne McLaurin, Paul M. Mathews, Ying Jiang, Stephen D. Schmidt, M. Azhar Chishti, Patrick Horne, Donna Heslin, Janet French, Howard T.J. Mount, Ralph A. Nixon, Marc Mercken, Catherine Bergeron, Paul E. Fraser, Peter St George-Hyslop () and David Westaway
Additional contact information
Christopher Janus: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
Jacqueline Pearson: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
JoAnne McLaurin: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
Paul M. Mathews: Nathan Kline Institute Center for Dementia Research, and New York University School of Medicine
Ying Jiang: Nathan Kline Institute Center for Dementia Research, and New York University School of Medicine
Stephen D. Schmidt: Nathan Kline Institute Center for Dementia Research, and New York University School of Medicine
M. Azhar Chishti: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
Patrick Horne: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
Donna Heslin: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
Janet French: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
Howard T.J. Mount: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
Ralph A. Nixon: Nathan Kline Institute Center for Dementia Research, and New York University School of Medicine
Marc Mercken: Janssen Research Foundation
Catherine Bergeron: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
Paul E. Fraser: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
Peter St George-Hyslop: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building
David Westaway: Centre for Research in Neurodegenerative Diseases, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Tanz Neuroscience Building

Nature, 2000, vol. 408, issue 6815, 979-982

Abstract: Abstract Much evidence indicates that abnormal processing and extracellular deposition of amyloid-β peptide (Aβ), a proteolytic derivative of the β-amyloid precursor protein (βAPP), 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 Aβ causes a marked reduction in burden of the brain amyloid2,3. Evidence that Aβ immunization also reduces cognitive dysfunction in murine models of Alzheimer's disease would support the hypothesis that abnormal Aβ 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 Aβ immunization reduces both deposition of cerebral fibrillar Aβ and cognitive dysfunction in the TgCRND8 murine model of Alzheimer's disease without, however, altering total levels of Aβ in the brain. This implies that either a ∼50% reduction in dense-cored Aβ plaques is sufficient to affect cognition, or that vaccination may modulate the activity/abundance of a small subpopulation of especially toxic Aβ species.

Date: 2000
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DOI: 10.1038/35050110

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