ReviewPathogens and disease2015
A brief history of prions.
Review in Pathogens and disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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
34 citing papers in PubMed.
- Epigenetic changes associated with the progression of prion disease in Syrian hamsters (Prion · 2026Article
- Article
- Impact of Chemical Aging on Venison Processing Knife Topography and Recoverable Chronic Wasting Disease Prion Seeding Activity.Pathogens (Basel, Switzerland) · 2026Article
- Quantifying Evidence for Competing Biomedical Hypotheses using Large Language Models and Bayesian Analysis.bioRxiv : the preprint server for biology · 2026Article
- Discovering, Integrating, and Reinterpreting the Molecular Logic of Life: From Classical Theories of Heredity to an Extended Functional Perspective on the Central Dogma.Life (Basel, Switzerland) · 2026Review
- Neurodegeneration as Ecosystem Failure: A New Paradigm for Prevention and Treatment.International journal of molecular sciences · 2025Review
- Epigenetic Changes Associated with the Progression of Prion Disease in Syrian Hamsters (Mesocricetus auratus).Research square · 2025Article
- Treatment with efavirenz extends survival in a Creutzfeldt-Jakob disease model by regulating brain cholesterol metabolism.JCI insight · 2025Article
- [SNG2], a prion form of Cut4/Apc1, confers non-Mendelian inheritance of heterochromatin silencing defect in fission yeast.Nucleic acids research · 2024Article
- Sleep disturbance in clinical and preclinical scrapie-infected sheep measured by polysomnography.The veterinary quarterly · 2024Article
- Article
- Heterozygosity for cervid S138N polymorphism results in subclinical CWD in gene-targeted mice and progressive inhibition of prion conversion.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The manifold role of octapeptide repeats in prion protein assembly.Peptide science (Hoboken, N.J.) · 2023Article
- Amyloidogenesis: What Do We Know So Far?International journal of molecular sciences · 2022Review
- Melatonin: Regulation of Prion Protein Phase Separation in Cancer Multidrug Resistance.Molecules (Basel, Switzerland) · 2022Review
- Prion Dissemination through the Environment and Medical Practices: Facts and Risks for Human Health.Clinical microbiology reviews · 2021Review
- microRNA-146a-5p, Neurotropic Viral Infection and Prion Disease (PrD).International journal of molecular sciences · 2021Review
- Viral and Prion Infections Associated with Central Nervous System Syndromes in Brazil.Viruses · 2021Review
- Review
- Effect of Scrapie Prion Infection in Ovine Bone Marrow-Derived Mesenchymal Stem Cells and Ovine Mesenchymal Stem Cell-Derived Neurons.Animals : an open access journal from MDPI · 2021Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteins were described as distinct biological molecules and their significance in cellular processes was recognized as early as the 18th century. At the same time, Spanish shepherds observed a disease that compelled their Merino sheep to pathologically scrape against fences, a defining clinical sign that led to the disease being named scrapie. In the late 19th century, Robert Koch published his postulates for defining causative agents of disease. In the early 20th century, pathologists Creutzfeldt and Jakob described a neurodegenerative disease that would later be included with scrapie into a group of diseases known as transmissible spongiform encephalopathies (TSEs). Later that century, mounting evidence compelled a handful of scientists to betray the prevailing biological dogma governing pathogen replication that Watson and Crick so convincingly explained by cracking the genetic code just two decades earlier. Because TSEs seemed to defy these new rules, J.S. Griffith theorized mechanisms by which a pathogenic protein could encipher its own replication blueprint without a genetic code. Stanley Prusiner called this proteinaceous infectious pathogen a prion. Here we offer a concise account of the discovery of prions, the causative agent of TSEs, in the wider context of protein biochemistry and infectious disease. We highlight the discovery of prions in yeast and discuss the implication of prions as epigenomic carriers of biological and pathological information. We also consider expanding the prion hypothesis to include other proteins whose alternate isoforms confer new biological or pathological properties.
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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.