Alzheimer's Disease Brain-Derived Amyloid-β-Mediated Inhibition of LTP In Vivo Is Prevented by Immunotargeting Cellular Prion Protein
Open accessAbstract
Synthetic amyloid-β protein (Aβ) oligomers bind with high affinity to cellular prion protein (PrP(C)), but the role of this interaction in mediating the disruption of synaptic plasticity by such soluble Aβ in vitro is controversial. Here we report that intracerebroventricular injection of Aβ-containing aqueous extracts of Alzheimer's disease (AD) brain robustly inhibits long-term potentiation (LTP) without significantly affecting baseline excitatory synaptic transmission in the rat hippocampus in vivo. Moreover, the disruption of LTP was abrogated by immunodepletion of Aβ. Importantly, intracerebroventricular administration of antigen-binding antibody fragment D13, directed to a putative Aβ-binding site on PrP(C), prevented the inhibition of LTP by AD brain-derived Aβ. In contrast, R1, a Fab directed to the C terminus of PrP(C), a region not implicated in binding of Aβ, did not significantly affect the Aβ-mediated inhibition of LTP. These data support the pathophysiological significance of SDS-stable Aβ dimer and the role of PrP(C) in mediating synaptic plasticity disruption by soluble Aβ.
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Small oligomers obtained from AD-affected human brain are active in plasticity assays.
“Small oligomers obtained from AD-affected human brain also are active in plasticity assays (Barry et al., 2011; Klyubin et al., 2008; Li et al., 2011).”
From The Aβ oligomer hypothesis for synapse failure and memory loss in Alzheimer’s disease (2011) · cites this paper as Barry et al., 2011
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References 35 · Cited by 237
- Authors
- Barry, A. E., Klyubin, I., Mc Donald, J. M., Mably, A. J., Farrell, M. A., Scott, M., Walsh, D. M., & Rowan, M. J.
- Affiliations
- Trinity College Dublin (IE)
- University College Dublin (IE)
- Beaumont Hospital (IE)
- Corresponding author
- Rowan, Michael J.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-05-18
- Volume
- 31
- Issue
- 20
- Pages
- 7259-7263
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6622598
- OpenAlex
- W2080670841
- Cited by
- 237
- References
- 35
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 4 · 2023: 6 · 2022: 11 · 2021: 17 · 2020: 6 · 2019: 13 · 2018: 14 · 2017: 18 · 2016: 14 · 2015: 25 · 2014: 24 · 2013: 37 · 2012: 28
- FWCI
- 22.26
- 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)
- Lenus, The Irish Health Repository (Dr Steevens Hospital Library) (submittedVersion)
- Funders
- Health Research Board
- European Commission (200611, 201159)
- Science Foundation Ireland (10/IN.1/B3001)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Keywords
- Alzheimer's disease, amyloid-beta, cellular prion protein, long-term potentiation, synaptic plasticity, hippocampus, soluble amyloid-beta oligomers, immunotargeting, antibody Fab fragment, intracerebroventricular administration, excitatory synaptic transmission
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Animals, Cerebral Cortex, Female, Hippocampus, Humans, Injections, Intraventricular, Male, Neural Inhibition, Neuronal Plasticity, Peptide Fragments, Amyloid beta-Peptides, Rats, Wistar, Long-Term Potentiation, PrPC Proteins, Rats
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