The DOI matches its Crossref record; 30 of the 31 references it cites were found in a registry or an index.
Prion protein and Aβ‐related synaptic toxicity impairment
Open accessAbstract
Alzheimer's disease (AD), the most common neurodegenerative disorder, goes along with extracellular amyloid-beta (Abeta) deposits. The cognitive decline observed during AD progression correlates with damaged spines, dendrites and synapses in hippocampus and cortex. Numerous studies have shown that Abeta oligomers, both synthetic and derived from cultures and AD brains, potently impair synaptic structure and functions. The cellular prion protein (PrP(C)) was proposed to mediate this effect. We report that ablation or overexpression of PrP(C) had no effect on the impairment of hippocampal synaptic plasticity in a transgenic model of AD. These findings challenge the role of PrP(C) as a mediator of Abeta toxicity.
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“other studies have shown that PrP-expressing and PrP-knockout mice are equally susceptible to long-term memory impairment induced by Aβ oligomers (Balducci et al., 2010; Calella et al., 2010)”
From The Aβ oligomer hypothesis for synapse failure and memory loss in Alzheimer’s disease (2011) · cites this paper as Calella et al., 2010
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1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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InfluentialCellular prion protein mediates impairment of synaptic plasticity by amyloid-β oligomers
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InfluentialMemory Impairment in Transgenic Alzheimer Mice Requires Cellular Prion Protein
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The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease
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Metadata
- Authors
- Calella, A. M., Farinelli, M., Nuvolone, M., Mirante, O., Moos, R., Falsig, J., Mansuy, I. M., & Aguzzi, A.
- Affiliations
- University Hospital Zurich (CH)
- University of Zurich (CH)
- University of Pavia (IT)
- Corresponding author
- Mansuy, Isabelle M.
- Aguzzi, Adriano
- Venue
- EMBO Molecular Medicine
- Published
- 2010-07-21
- Volume
- 2
- Issue
- 8
- Pages
- 306-314
- ISSN
- 1757-4676 (ISSN-L)
- 1757-4684
- PMC
- PMC2962809
- OpenAlex
- W2131558033
- Cited by
- 242
- References
- 31
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 4 · 2022: 10 · 2021: 13 · 2020: 9 · 2019: 7 · 2018: 11 · 2017: 18 · 2016: 19 · 2015: 23 · 2014: 18 · 2013: 30 · 2012: 30
- FWCI
- 22.74
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- EMBO Molecular Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, cc-by)
- Repository for Publications and Research Data (ETH Zurich) (submittedVersion, cc-by)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by)
- ETH Zürich Research Collection (cc-by)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- Novartis Foundation
- European Commission
- National Research Foundation
- Collegio Ghislieri di Pavia
- Schweizerische Akademie der Medizinischen Wissenschaften
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- cellular prion protein, amyloid-beta oligomers, synaptic toxicity, Alzheimer's disease, synaptic plasticity, hippocampus, transgenic mouse model, synapse damage
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Hippocampus, Humans, Mice, Transgenic, Prions, Synapses, Amyloid beta-Peptides, Mice
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