ArticleNature neuroscience2012
Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons.
Article in Nature neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 383 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
383 citing papers in PubMed, 640 citations in OpenAlex.
- Fyn kinase: a key mechanistic regulator and therapeutic target in tauopathy and neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Protein Aggregates as Drivers of Receptor Clustering and Pathological Signaling: A Framework Linking Extracellular Amyloid-β to Tau Dysregulation.ACS chemical neuroscience · 2026Review
- Article
- Role of prion protein in mediating the synaptotoxic effects of tau oligomers: Implications for Alzheimer's disease and related tauopathies.Neural regeneration research · 2026Article
- Tau physiology and pathology: impacts on cellular structures and neurodegenerative diseases.Inflammopharmacology · 2026Review
- Distinct Filament Conformation for Receptor-Bound Amyloid-β from Alzheimer's Disease Brain.Nature communications · 2026Article
- The Effect of CuACS chemical neuroscience · 2026Article
- The Genetic and Transcriptomic Nexus of Age-Related Hearing Loss and Alzheimer's Disease.Genes · 2026Article
- Cellular prion protein and its derived peptides: multifaceted roles in neurodegenerative diseases and potential as biomarkers.Cell & bioscience · 2026Review
- PrPStem cell reports · 2026Article
- High glucose levels sensitize neuron-like cells to damage induced by oxidative and neurotoxic agents.Scientific reports · 2026Article
- Early onset Alzheimer's disease with V180I variant of prion protein gene and a family history of dementia: a case report.BMC neurology · 2026Article
- The interactions of copper, glutamate, and cuproptosis: insights into brain health and Alzheimer's disease pathology.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Protein kinases as therapeutic targets in Alzheimer's disease: challenges, insights, and new frontiers.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- Review
- Amyloid Beta Oligomers as Early Triggers of Neuronal Cytoskeleton Dysfunction in Alzheimer's Disease.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- A phase separation hypothesis for the biological function of PrP: the role of multivalent interactions at the plasma membrane.Biochemical Society transactions · 2026Review
- APOE genotype differentially modulates prion pathology in a mouse model.Acta neuropathologica communications · 2026Article
- Selective vulnerability of the aging cholinergic system to amyloid pathology revealed by induced APP overexpression.Journal of neuroinflammation · 2026Article
- Role of Mitochondrial Calcium Dysregulation in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2025Review
323 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Amyloid-beta (Aβ) oligomers are thought to trigger Alzheimer's disease pathophysiology. Cellular prion protein (PrP(C)) selectively binds oligomeric Aβ and can mediate Alzheimer's disease-related phenotypes. We examined the specificity, distribution and signaling of Aβ-PrP(C) complexes, seeking to understand how they might alter the function of NMDA receptors (NMDARs) in neurons. PrP(C) is enriched in postsynaptic densities, and Aβ-PrP(C) interaction leads to Fyn kinase activation. Soluble Aβ assemblies derived from the brains of individuals with Alzheimer's disease interacted with PrP(C) to activate Fyn. Aβ engagement of PrP(C)-Fyn signaling yielded phosphorylation of the NR2B subunit of NMDARs, which was coupled to an initial increase and then a loss of surface NMDARs. Aβ-induced dendritic spine loss and lactate dehydrogenase release required both PrP(C) and Fyn, and human familial Alzheimer's disease transgene-induced convulsive seizures did not occur in mice lacking PrP(C). These results delineate an Aβ oligomer signal transduction pathway that requires PrP(C) and Fyn to alter synaptic function, with deleterious consequences in Alzheimer's disease.
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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.