ArticleJournal of proteome research2014
Proteomics analysis of amyloid and nonamyloid prion disease phenotypes reveals both common and divergent mechanisms of neuropathogenesis.
Article in Journal of proteome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Multiomic analyses direct hypotheses for Creutzfeldt-Jakob disease risk genes.Brain : a journal of neurology · 2025Article
- Trazodone rescues dysregulated synaptic and mitochondrial nascent proteomes in prion neurodegeneration.Brain : a journal of neurology · 2024Article
- The PINK1/Parkin pathway of mitophagy exerts a protective effect during prion disease.PloS one · 2024Article
- Potential Prion Involvement in Long COVID-19 Neuropathology, Including Behavior.Cellular and molecular neurobiology · 2023Review
- Redox mechanisms and their pathological role in prion diseases: The road to ruin.PLoS pathogens · 2023Review
- Cryo-EM structures of prion protein filaments from Gerstmann-Sträussler-Scheinker disease.Acta neuropathologica · 2022Article
- Article
- The characterization of AD/PART co-pathology in CJD suggests independent pathogenic mechanisms and no cross-seeding between misfolded Aβ and prion proteins.Acta neuropathologica communications · 2019Article
- Generation and propagation of yeast prion [URE3] are elevated under electromagnetic field.Cell stress & chaperones · 2018Article
- Mitochondrial Respiration Is Impaired during Late-Stage Hamster Prion Infection.Journal of virology · 2017Article
- Cellular prion protein is present in mitochondria of healthy mice.Scientific reports · 2017Article
- Application of "Omics" Technologies for Diagnosis and Pathogenesis of Neurological Infections.Current neurology and neuroscience reports · 2015Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Prion diseases are a heterogeneous group of neurodegenerative disorders affecting various mammals including humans. Prion diseases are characterized by a misfolding of the host-encoded prion protein (PrP(C)) into a pathological isoform termed PrP(Sc). In wild-type mice, PrP(C) is attached to the plasma membrane by a glycosylphosphatidylinositol (GPI) anchor and PrP(Sc) typically accumulates in diffuse nonamyloid deposits with gray matter spongiosis. By contrast, when mice lacking the GPI anchor are infected with the same prion inoculum, PrP(Sc) accumulates in dense perivascular amyloid plaques with little or no gray matter spongiosis. In order to evaluate whether different host biochemical pathways were implicated in these two phenotypically distinct prion disease models, we utilized a proteomics approach. In both models, infected mice displayed evidence of a neuroinflammatory response and complement activation. Proteins involved in cell death and calcium homeostasis were also identified in both phenotypes. However, mitochondrial pathways of apoptosis were implicated only in the nonamyloid form, whereas metal binding and synaptic vesicle transport were more disrupted in the amyloid phenotype. Thus, following infection with a single prion strain, PrP(C) anchoring to the plasma membrane correlated not only with the type of PrP(Sc) deposition but also with unique biochemical pathways associated with pathogenesis.
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