β-Amyloid Immunotherapy Prevents Synaptic Degeneration in a Mouse Model of Alzheimer's Disease
Open accessAbstract
Alzheimer's disease neuropathology is characterized by key features that include the deposition of the amyloid β peptide (Aβ) into plaques, the formation of neurofibrillary tangles, and the loss of neurons and synapses in specific brain regions. The loss of synapses, and particularly the associated presynaptic vesicle protein synaptophysin in the hippocampus and association cortices, has been widely reported to be one of the most robust correlates of Alzheimer's disease-associated cognitive decline. The β-amyloid hypothesis supports the idea that Aβ is the cause of these pathologies. However, the hypothesis is still controversial, in part because the direct role of Aβ in synaptic degeneration awaits confirmation. In this study, we show that Aβ reduction by active or passive Aβ immunization protects against the progressive loss of synaptophysin in the hippocampal molecular layer and frontal neocortex of a transgenic mouse model of Alzheimer's disease. These results, substantiated by quantitative electron microscopic analysis of synaptic densities, strongly support a direct causative role of Aβ in the synaptic degeneration seen in Alzheimer's disease and strengthen the potential of Aβ immunotherapy as a treatment approach for this disease.
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In preclinical studies, the murine form of the antibody 3D6 reduces the amount of Aβ in the brain.
“In preclinical studies, the murine form of the antibody (3D6) was shown to bind to fibrillar, oligomeric, and monomeric forms of Aβ, reduce the amount of Aβ in the brain, and improve memory in transgenic mice that overproduced Aβ.4–8”
From Two Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Alzheimer's Disease (2014) · cites this paper as [6]
In preclinical studies, the murine form of the antibody 3D6 binds fibrillar, oligomeric, and monomeric forms of Aβ.
“In preclinical studies, the murine form of the antibody (3D6) was shown to bind to fibrillar, oligomeric, and monomeric forms of Aβ, reduce the amount of Aβ in the brain, and improve memory in transgenic mice that overproduced Aβ.4–8”
From Two Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Alzheimer's Disease (2014) · cites this paper as [6]
In preclinical studies, the murine form of the antibody 3D6 improves memory in transgenic mice that overproduce Aβ.
“In preclinical studies, the murine form of the antibody (3D6) was shown to bind to fibrillar, oligomeric, and monomeric forms of Aβ, reduce the amount of Aβ in the brain, and improve memory in transgenic mice that overproduced Aβ.4–8”
From Two Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Alzheimer's Disease (2014) · cites this paper as [6]
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Self-citation
- Authors
- Buttini, M., Masliah, E., Barbour, R., Grajeda, H., Motter, R., Johnson-Wood, K., Khan, K., Seubert, P., Freedman, S., Schenk, D., & Games, D.
- Affiliations
- Elan Pharmaceuticals, Inc. (Ireland) (IE)
- University of California San Diego (US)
- Corresponding author
- Buttini, Manuel
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2005-10-05
- Volume
- 25
- Issue
- 40
- Pages
- 9096-9101
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6725749
- OpenAlex
- W2149086197
- Cited by
- 176
- References
- 43
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 4 · 2023: 4 · 2022: 3 · 2021: 6 · 2020: 8 · 2019: 4 · 2018: 6 · 2017: 5 · 2016: 8 · 2015: 8 · 2014: 12 · 2013: 6 · 2012: 11
- FWCI
- 9.79
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, amyloid-beta, synaptic degeneration, synaptophysin, hippocampus, frontal neocortex, transgenic mouse model, synaptic density, cognitive decline
- MeSH terms
- Age Factors, Alzheimer Disease, Animals, Cerebral Cortex, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Hippocampus, Immunohistochemistry, Immunotherapy, Mice, Transgenic, Nerve Degeneration, Peptides, Synapses, Amyloid beta-Peptides, Synaptophysin, Mice
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