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

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

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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  • PrP-expressing and PrP-knockout mice are equally susceptible to long-term memory impairment induced by Aβ oligomers.

    “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)”

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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
Venue
EMBO Molecular Medicine
Published
2010-07-21
Volume
2
Issue
8
Pages
306-314
ISSN
  • 1757-4676 (ISSN-L)
  • 1757-4684
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
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
  • Health Sciences › Medicine › Physiology › 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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