ArticlePloS one2015
Treatment of Prion Disease with Heterologous Prion Proteins.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 21 citations in OpenAlex.
- Prion diseases disrupt glutamate/glutamine metabolism in skeletal muscle.PLoS pathogens · 2024Article
- Recombinant ovine prion protein can be mutated at position 136 to improve its efficacy as an inhibitor of prion propagation.Scientific reports · 2023Article
- Aminoquinolones and Their Benzoquinone Dimer Hybrids as Modulators of Prion Protein Conversion.Molecules (Basel, Switzerland) · 2022Article
- Applications of Various Types of Nanomaterials for the Treatment of Neurological Disorders.Nanomaterials (Basel, Switzerland) · 2022Review
- The role of prion strain diversity in the development of successful therapeutic treatments.Progress in molecular biology and translational science · 2020Review
- Nonpathogenic Heterologous Prions Can Interfere with Prion Infection in a Strain-Dependent Manner.Journal of virology · 2018Article
- Recombinant PrP and Its Contribution to Research on Transmissible Spongiform Encephalopathies.Pathogens (Basel, Switzerland) · 2017Review
- Reduced Abundance and Subverted Functions of Proteins in Prion-Like Diseases: Gained Functions Fascinate but Lost Functions Affect Aetiology.International journal of molecular sciences · 2017Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Prion diseases such as Creutzfeldt-Jakob disease in humans, bovine spongiform encephalopathy in cattle, and scrapie in sheep are fatal neurodegenerative diseases for which there is no effective treatment. The pathology of these diseases involves the conversion of a protease sensitive form of the cellular prion protein (PrPC) into a protease resistant infectious form (PrPsc or PrPres). Both in vitro (cell culture and cell free conversion assays) and in vivo (animal) studies have demonstrated the strong dependence of this conversion process on protein sequence homology between the initial prion inoculum and the host's own cellular prion protein. The presence of non-homologous (heterologous) proteins is often inhibitory to this conversion process. We hypothesize that the presence of heterologous prion proteins from one species might therefore constitute an effective treatment for prion disease in another species. To test this hypothesis, we infected mice intracerebrally with murine adapted RML-Chandler scrapie and treated them with heterologous prion protein (purified bacterially expressed recombinant hamster prion protein) or vehicle alone. Treated animals demonstrated reduced disease associated pathology, decreased accumulation of protease-resistant disease-associated prion protein, with delayed onset of clinical symptoms and motor deficits. This was concomitant with significantly increased survival times relative to mock-treated animals. These results provide proof of principle that recombinant hamster prion proteins can effectively and safely inhibit prion disease in mice, and suggest that hamster or other non-human prion proteins may be a viable treatment for prion diseases in humans.
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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.