Cited by 242Alzheimer's disease research and treatmentsPrion Diseases and Protein MisfoldingNeuroscience and Neuropharmacology Research

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Prion protein and Aβ‐related synaptic toxicity impairment

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Calella, Anna Maria, Farinelli, Mélissa, Nuvolone, Mario, Mirante, Osvaldo, Moos, Rita, Falsig, Jeppe, Mansuy, Isabelle M., Aguzzi, Adriano·2010·EMBO Molecular Medicine

DOI 10.1002/emmm.201000082PMC PMC2962809

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Abstract

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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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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“…Ab exists in AD brains as a vastly heterodisperse spectrum of assemblies ranging from monomers and dimers to oligomers and extremely large fibrillary aggregates, each one of which may partly contribute to the AD phenotype (Lesne et al, 2006; Shankar et al, 2008, 2009; Walsh et al, 2002).”
Retracted
Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory
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Normal development and behaviour of mice lacking the neuronal cell-surface PrP protein
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“PrPC concentration was determined by sandwich ELISA as described (Polymenidou et al, 2008).”
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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
ORCID: Farinelli, Mélissa
Nuvolone, Mario
Mansuy, Isabelle M.
Aguzzi, Adriano
Venue: EMBO Molecular Medicine
Publisher: Springer Science and Business Media LLC
Published: 2010-07-21
Volume: 2
Issue: 8
Pages: 306-314
ISSN: 1757-4676 (ISSN-L)
1757-4684
DOI: 10.1002/emmm.201000082
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
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
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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Prion protein and Aβ‐related synaptic toxicity impairment

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