ArticleProceedings of the National Academy of Sciences of the United States of America2002
Transmission of prions.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.
- Risk of transmission of sporadic Creutzfeldt-Jakob disease by surgical procedures: systematic reviews and quality of evidence.Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2017Pooled it
- Inborn errors of canonical autophagy in neurodegenerative diseases.Human molecular genetics · 2025Review
- Structural and dynamical determinants of a β-sheet-enriched intermediate involved in amyloid fibrillar assembly of human prion protein.Chemical science · 2022Article
- Reverse engineering Lewy bodies: how far have we come and how far can we go?Nature reviews. Neuroscience · 2021Review
- Transition of the prion protein from a structured cellular form (PrPProtein science : a publication of the Protein Society · 2019Review
- Spatial heterogeneity of prion gene polymorphisms in an area recently infected by chronic wasting disease.Prion · 2019Article
- Cellular mechanisms responsible for cell-to-cell spreading of prions.Cellular and molecular life sciences : CMLS · 2018Review
- Ex vivo mammalian prions are formed of paired double helical prion protein fibrils.Open biology · 2016Article
- Etiologic Framework for the Study of Neurodegenerative Disorders as Well as Vascular and Metabolic Comorbidities on the Grounds of Shared Epidemiologic and Biologic Features.Frontiers in aging neuroscience · 2016Article
- Disruption of glycosylation enhances ubiquitin-mediated proteasomal degradation of Shadoo in Scrapie-infected rodents and cultured cells.Molecular neurobiology · 2014Article
- Cell-to-cell transmission of pathogenic proteins in neurodegenerative diseases.Nature medicine · 2014Review
- Towards an age-dependent transmission model of acquired and sporadic Creutzfeldt-Jakob disease.PloS one · 2014Article
- Late-in-life surgery associated with Creutzfeldt-Jakob disease: a methodological outline for evidence-based guidance.Emerging themes in epidemiology · 2013Article
- Structural plasticity of the cellular prion protein and implications in health and disease.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Exosomes as intercellular signaling organelles involved in health and disease: basic science and clinical applications.International journal of molecular sciences · 2013Article
- Use of transgenic animals in biotechnology: prospects and problems.Acta naturae · 2013Article
- QSAR study of anti-prion activity of 2-aminothiazoles.EXCLI journal · 2012Article
- Protease-resistant prions selectively decrease Shadoo protein.PLoS pathogens · 2011Article
- Decreased CSF transferrin in sCJD: a potential pre-mortem diagnostic test for prion disorders.PloS one · 2011Article
- Spontaneous generation of mammalian prions.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The "protein only" hypothesis states that the infectious agent causing transmissible spongiform encephalopathies is a conformational isomer of PrP, a host protein predominantly expressed in brain, and is strongly supported by many lines of evidence. Prion diseases are so far unique among conformational diseases in that they are transmissible, not only experimentally but also by natural routes, mainly by ingestion. A striking feature of prions is their extraordinary resistance to conventional sterilization procedures, and their capacity to bind to surfaces of metal and plastic without losing infectivity. This property, first observed in a clinical setting, is now being investigated in experimental settings, both in animals and in cell culture.
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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.