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Anti-Aβ antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice
Open accessAbstract
Neuritic plaques are a defining feature of Alzheimer disease (AD) pathology. These structures are composed of extracellular accumulations of amyloid-beta peptide (Abeta) and other plaque-associated proteins, surrounded by large, swollen axons and dendrites (dystrophic neurites) and activated glia. Dystrophic neurites are thought to disrupt neuronal function, but whether this damage is static, dynamic, or reversible is unknown. To address this, we monitored neuritic plaques in the brains of living PDAPP;Thy-1:YFP transgenic mice, a model that develops AD-like pathology and also stably expresses yellow fluorescent protein (YFP) in a subset of neurons in the brain. Using multiphoton microscopy, we observed and monitored amyloid through cranial windows in PDAPP;Thy-1:YFP double-transgenic mice using the in vivo amyloid-imaging fluorophore methoxy-X04, and individual YFP-labeled dystrophic neurites by their inherent fluorescence. In vivo studies using this system suggest that amyloid-associated dystrophic neurites are relatively stable structures in PDAPP;Thy-1:YFP transgenic mice over several days. However, a significant reduction in the number and size of dystrophic neurites was seen 3 days after Abeta deposits were cleared by anti-Abeta antibody treatment. This analysis suggests that ongoing axonal and dendritic damage is secondary to Abeta and is, in part, rapidly reversible.
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“and even rapidly resolve some of the neuritic swellings near plaques (Brendza et al., 2005).”
From Dendritic Spine Abnormalities in Amyloid Precursor Protein Transgenic Mice Demonstrated by Gene Transfer and Intravital Multiphoton Microscopy (2005) · cites this paper as Brendza et al., 2005
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“We have recently demonstrated that treatment with anti-Aβ antibodies in APP transgenic mice can remove plaques (Bacskai et al., 2002), straighten the trajectory of neurites (Lombardo et al., 2003) and even rapidly resolve some of the neuritic swellings near plaques (Brendza et al., 2005).”
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Metadata
- Authors
- Brendza, R. P., Bacskai, B. J., Cirrito, J. R., Simmons, K. A., Skoch, J. M., Klunk, W. E., Mathis, C. A., Bales, K. R., Paul, S. M., Hyman, B. T., & Holtzman, D. M.
- Affiliations
- Washington University in St. Louis (US)
- Harvard University (US)
- University of Pittsburgh (US)
- Eli Lilly (United States) (US)
- Corresponding author
- Holtzman, David M.
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2005-01-20
- Volume
- 115
- Issue
- 2
- Pages
- 428-433
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC544607
- OpenAlex
- W2126885422
- Cited by
- 190
- References
- 10
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 5 · 2023: 4 · 2022: 2 · 2021: 4 · 2020: 4 · 2019: 2 · 2017: 5 · 2016: 5 · 2015: 5 · 2014: 2 · 2013: 10 · 2012: 7
- FWCI
- 15.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Funders
- Alzheimer's Association (EB00768, AG13956)
- American Health Assistance Foundation
- Eli Lilly and Company
- National Institutes of Health (AG13956, AG08487)
- National Institute on Aging (AG20222, AG-08487, R01AG020222, R01AG013956, R01AG008487, R01AG020570, R37AG013956, AG13956, AG 020570)
- National Institute of Neurological Disorders and Stroke (P01NS032636)
- National Institute of Biomedical Imaging and Bioengineering (EB-00768, R01EB000768)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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
- amyloid-beta, neuritic plaques, dystrophic neurites, Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Animals, Antibodies, Monoclonal, Mice, Transgenic, Radiography, Neurites, Amyloid beta-Protein Precursor, Neuroaxonal Dystrophies, Tomography, Optical, Mice, Plaque, Amyloid
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