ArticlePLoS pathogens2020
Mutant prion proteins increase calcium permeability of AMPA receptors, exacerbating excitotoxicity.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Memantine inhibits calcium-permeable AMPA receptors.Nature communications · 2025Article
- Mutant prion protein enhances NMDA receptor activity, activates PKC, and triggers rapid excitotoxicity in mice.The Journal of clinical investigation · 2025Article
- Cannabinoids as Multitarget Drugs for the Treatment of Autoimmunity in Glaucoma.ACS pharmacology & translational science · 2025Review
- New Light on Prions: Putative Role of PrPInternational journal of molecular sciences · 2024Review
- Mechanisms of prion-induced toxicity.Cell and tissue research · 2023Review
- Reelin and APP Cooperatively Modulate Dendritic Spine FormationExperimental neurobiology · 2023Article
- Article
- Neurons and Astrocytes Elicit Brain Region Specific Transcriptional Responses to Prion Disease in the Murine CA1 and Thalamus.Frontiers in neuroscience · 2022Article
- Neuronal excitatory-to-inhibitory balance is altered in cerebral organoid models of genetic neurological diseases.Molecular brain · 2021Article
- Amyloid Prefibrillar Oligomers: The Surprising Commonalities in Their Structure and Activity.International journal of molecular sciences · 2021Review
- CaThe Journal of physiology · 2021Article
- Calcium Permeable-AMPA Receptors and Excitotoxicity in Neurological Disorders.Frontiers in neural circuits · 2021Review
- PrPFrontiers in molecular neuroscience · 2021Review
- Correction: Mutant prion proteins increase calcium permeability of AMPA receptors, exacerbating excitotoxicity.PLoS pathogens · 2020Article
- Activation of Src family kinase ameliorates secretory trafficking in mutant prion protein cells.The Journal of biological chemistryArticle
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion protein (PrP) mutations are linked to genetic prion diseases, a class of phenotypically heterogeneous neurodegenerative disorders with invariably fatal outcome. How mutant PrP triggers neurodegeneration is not known. Synaptic dysfunction precedes neuronal loss but it is not clear whether, and through which mechanisms, disruption of synaptic activity ultimately leads to neuronal death. Here we show that mutant PrP impairs the secretory trafficking of AMPA receptors (AMPARs). Specifically, intracellular retention of the GluA2 subunit results in synaptic exposure of GluA2-lacking, calcium-permeable AMPARs, leading to increased calcium permeability and enhanced sensitivity to excitotoxic cell death. Mutant PrPs linked to different genetic prion diseases affect AMPAR trafficking and function in different ways. Our findings identify AMPARs as pathogenic targets in genetic prion diseases, and support the involvement of excitotoxicity in neurodegeneration. They also suggest a mechanistic explanation for how different mutant PrPs may cause distinct disease phenotypes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.