ArticleActa neuropathologica2020
Prevalence in Britain of abnormal prion protein in human appendices before and after exposure to the cattle BSE epizootic.
Article in Acta neuropathologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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27 citing papers in PubMed, 61 citations in OpenAlex.
- Formic acid treatment drastically reduces sporadic Creutzfeldt-Jakob disease and variant Creutzfeldt-Jakob disease infectivity in histological samples as tested in a high-sensitivity mouse bioassay.The Journal of general virology · 2026Article
- Strain-specific propagation of variant Creutzfeldt-Jakob disease prions in humanized neural cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Estimating future variant Creutzfeldt-Jakob disease cases in the UK: a cohort-based probabilistic model.The Lancet regional health. Europe · 2025Article
- Article
- No evidence of subclinical infection in sheep surviving oral challenge with prions.The Journal of general virology · 2025Article
- Isolation of a novel human prion strain from a PRNP codon 129 heterozygous vCJD patient.PLoS pathogens · 2025Article
- Bovine spongiform encephalopathy: A review of current knowledge and challenges.Open veterinary journal · 2025Review
- Abnormal Expression of Proteolytic Stress-Related Proteins and Protective Effect of Fibrinolytic Enzymes in Prion Diseases.Transboundary and emerging diseases · 2025Article
- Biomarker-Based Approach to α-Synucleinopathies: Lessons from Neuropathology.Movement disorders : official journal of the Movement Disorder Society · 2024Article
- Article
- BSE risk posed by ruminant collagen and gelatine derived from bones.EFSA journal. European Food Safety Authority · 2024Article
- Lack of Transmission of Chronic Wasting Disease Prions to Human Cerebral Organoids.Emerging infectious diseases · 2024Article
- Conservation of vCJD Strain Properties After Extraction and In Vitro Propagation of PrPMolecular neurobiology · 2023Article
- Non-human primates in prion diseases.Cell and tissue research · 2023Review
- Prion assemblies: structural heterogeneity, mechanisms of formation, and role in species barrier.Cell and tissue research · 2023Review
- Human prion diseases and the prion protein - what is the current state of knowledge?Translational neuroscience · 2023Review
- Risk of variant Creutzfeldt-Jakob disease transmission by blood transfusion in Australia.Vox sanguinis · 2022Article
- A clinicopathological study of selected cognitive impairment cases in Lothian, Scotland: enhanced CJD surveillance in the 65 + population group.BMC geriatrics · 2022Article
- The First Evaluation of Proteinase K-Resistant Prion Protein (PrPMedicina (Kaunas, Lithuania) · 2022Article
- Genetic aspects of human prion diseases.Frontiers in neurology · 2022Review
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Authors and funding
19 authors at 6 institutions in 1 country.
Funding
Abstract
Widespread dietary exposure of the population of Britain to bovine spongiform encephalopathy (BSE) prions in the 1980s and 1990s led to the emergence of variant Creutzfeldt-Jakob Disease (vCJD) in humans. Two previous appendectomy sample surveys (Appendix-1 and -2) estimated the prevalence of abnormal prion protein (PrP) in the British population exposed to BSE to be 237 per million and 493 per million, respectively. The Appendix-3 survey was recommended to measure the prevalence of abnormal PrP in population groups thought to have been unexposed to BSE. Immunohistochemistry for abnormal PrP was performed on 29,516 samples from appendices removed between 1962 and 1979 from persons born between 1891 through 1965, and from those born after 1996 that had been operated on from 2000 through 2014. Seven appendices were positive for abnormal PrP, of which two were from the pre-BSE-exposure era and five from the post BSE-exposure period. None of the seven positive samples were from appendices removed before 1977, or in patients born after 2000 and none came from individuals diagnosed with vCJD. There was no statistical difference in the prevalence of abnormal PrP across birth and exposure cohorts. Two interpretations are possible. Either there is a low background prevalence of abnormal PrP in human lymphoid tissues that may not progress to vCJD. Alternatively, all positive specimens are attributable to BSE exposure, a finding that would necessitate human exposure having begun in the late 1970s and continuing through the late 1990s.
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