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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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“…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).”
RetractedShankar, G. M., Li, S., Mehta, T. H., Garcia-Munoz, A., Shepardson, N. E., Smith, I., Brett, F. M., Farrell, M. A., Rowan, M. J., Lemere, C. A., et al. (2008) · Nature Medicine · doi:10.1038/nm1782 · Cited by 3,685
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“PrPC concentration was determined by sandwich ELISA as described (Polymenidou et al, 2008).”
InfluentialCellular prion protein mediates impairment of synaptic plasticity by amyloid-β oligomers
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LRP/Amyloid β-Peptide Interaction Mediates Differential Brain Efflux of Aβ Isoforms
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Items 201–242 of 242
Striatal pathology underlies prion infection-mediated hyperactivity in mice
Gunapala, K. M., Chang, D., Hsu, C. T., Manaye, K. F., Drenan, R. M., Switzer, R. C., & Steele, A. D. (2010) · Prion · doi:10.4161/pri.4.4.13721 · Cited by 8
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Tau Exon 10 Inclusion by PrPC through Downregulating GSK3β Activity
Lidón, L., Llaó-Hierro, L., Nuvolone, M., Aguzzi, A., Ávila, J., Ferrer, I., del Rı́o, J. A., & Gavı́n, R. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22105370 · Cited by 6
Boroujeni, E. R., Hosseini, S. M., Fani, G., Cecchi, C., & Chiti, F. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21197273 · Cited by 7
Cellular prion protein offers neuroprotection in astrocytes submitted to amyloid β oligomer toxicity
Marques, C. M. S., Gomes, R. N., Pedron, T., Batista, B. L., & Cerchiaro, G. (2022) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-022-04631-w · Cited by 6
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Smid, J., Landemberger, M. C., Bahia, V. S., Martins, V. R., & Nitríni, R. (2013) · Arquivos de Neuro-Psiquiatria · doi:10.1590/0004-282x20130055 · Cited by 6
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Cholesterol and Fat Metabolism in Alzheimer’s Disease
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New light on prions: putative role of co-operation of PrPc and Aβ proteins in cognition
Chrobak, A. A., & Adamek, D. (2014) · Folia Neuropathologica · doi:10.5114/fn.2014.41739 · Cited by 5
The pathogenesis of soluble PrP fragments containing Aβ binding sites
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Targeting Aβ Receptors to Modify Alzheimer’s Disease Progression
Haas, L. T., & Strittmatter, S. M. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-802173-6.00008-3 · Cited by 2
Zhao, J., Ma, B., & Nussinov, R. (2016) · Israel Journal of Chemistry · doi:10.1002/ijch.201600093 · Cited by 2
Inhibitors of Tau-Phosphorylating Kinases
Fallacara, A. L., Trist, I. M. L., Schenone, S., & Botta, M. (2017) · Topics in medicinal chemistry · doi:10.1007/7355_2016_17 · Cited by 2
Cellular prion protein and calcium ions trigger the neurotoxicity of α-synuclein aggregates
Bigi, A., Conti, A. C., Napolitano, L., Fusco, G., Simone, A. D., Chiti, F., Cascella, R., & Cecchi, C. (2025) · Cell & Bioscience · doi:10.1186/s13578-025-01479-7 · Cited by 1
Amyloidy i prionoidy – czy jest już czas, żeby się obawiać?
Liberski, P. P. (2013) · DOAJ (DOAJ: Directory of Open Access Journals) · Cited by 1
Effects of FlAsH/Tetracysteine (TC) Tag on PrP Proteolysis and PrPres Formation by TC‐Scanning
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Biological Targeting and Activity of Pre-fibrillar Aβ Assemblies
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The Cellular Prion Protein as Universal Receptor for Amyloid Proteins
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Wang, Y., & Xue, L. (2014) · Advances in Alzheimer s Disease · doi:10.4236/aad.2014.31003 · Cited by 1
Role of Cellular Prion Protein in the Amyloid-β Oligomer Pathophysiology of Alzheimer’s Disease
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Poliformismos do gene da proteína príon celular em pacientes com doença de Alzheimer
Smid, J. (2011) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.5.2011.tde-24052011-142607
REMOVED: Acute depletion of the prion protein may abrogate Aβ oligomer toxicity
Radford, H. E., Verity, N. C., Martin, M. G., & Mallucci, G. R. (2011) · Toxicology · doi:10.1016/j.tox.2011.09.043
RetractedNeuropathogenesis of Prion Disease
Davidson, L., & Knight, R. (2014) · Future Neurology · doi:10.2217/fnl.13.74
Review: prion protein and amyloid beta interactions
Minikel, E. V. (2013)
Does glimepiride provide a novel mechanism of neutralising toxic amyloid-β?
(2016) · Neuroscience Communications · doi:10.14800/nc.1197
New Small Molecule Drug Discovery for Alzheimer's Disease
Liu, K., Zhang, M., & Nagappan, G. (2012) · Frontiers in neuroscience · doi:10.1201/b11986-6
Investigating the functional roles of microRNA-29b and microRNA-146a in prion diseases
Zhao, W. (2018) · Minerva Access (University of Melbourne)
Béringue, V. (2015) · Reviews in Cell Biology and Molecular Medicine · doi:10.1002/3527600906.mcb.200400151.pub2
Alzheimer’s disease as a syndrome of overloaded amyloidic synaptic tagging in memory networksPreprint
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Evaluation expérimentale du risque prion lié aux porteurs asymptomatiques chez l'Homme et le macaque
Rontard, J. (2018) · theses.fr (ABES) · doi:10.70675/ee7dac13zd082z49c7za670z3e9b627c4ab7
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PrPC limits APP delivery to the plasma membrane and alters its processing to facilitate Aβ release
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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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