ReviewProceedings of the National Academy of Sciences of the United States of America1998
Prions.
Review in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00183092 (Novel Therapeutics For Prion Diseases), which is not on this map. Cited by 2,286 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Novel Therapeutics For Prion Diseases: A Randomized, Double-blinded, Placebo-controlled Study of the Efficacy of Quinacrine in the Treatment of Sporadic Creutzfeldt-Jakob Disease
Who cites it
2,286 citing papers in PubMed, 5,339 citations in OpenAlex.
- Inferring Geographic Origin of White-Tailed Deer (Ecology and evolution · 2026Article
- Article
- Piano-Stool Ru (II) Complexes as Modulators of Human Prion Protein PrPChemMedChem · 2026Article
- Concise Total Synthesis and Pharmacological Evaluation of Procerones A and B.ACS pharmacology & translational science · 2026Article
- Article
- Leveraging the dominant-negative effect of the kuru-protective G127V prion protein variant as a novel therapeutic strategy.Neurobiology of disease · 2026Article
- Phenotypic screening for small molecules that lower PrP in cultured cells.Molecular and cellular neurosciences · 2026Article
- Interferon-Stimulated Gene-Mediated Defense Against Prion Infection: Noncanonical Function of Oas1a.Viruses · 2026Review
- Endogenous Ecotropic Murine Leukemia Virus Promotes Prion Pathogenesis in Senescence-accelerated Mice.Experimental neurobiology · 2026Article
- BoDV-1 Infection Is Associated with Altered Prion Protein Glycoform Maturation and Reduced ETS1-MGAT5/GnTV Pathway Activity in Rat C6 Astroglial Cells.Microorganisms · 2026Article
- A neural stem cell-derived 3D spheroid model that recapitulates prion infection and pathology.Materials today. Bio · 2026Article
- 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
- A self-complementary recombinant adeno-associated virus vector coding for an anchorless prion protein carrying the G127V mutation extends survival in a rodent prion disease model.PLoS pathogens · 2026Article
- Protein-First, but Not Protein-Only: Rethinking Neurodegenerative Diseases Through Transgenic Mouse Models.Neurology international · 2026Article
- A scalable, dividing cell model for the robust propagation and quantification of human sporadic Creutzfeldt-Jakob disease prions.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The amyloid packing difference: A pairwise comparison metric for amyloid structures.Structure (London, England : 1993) · 2026Article
- Prion propagation is controlled by discrete structural regions of PrP rather than overall stability.The Journal of biological chemistry · 2026Article
- QBP1 Peptide as a Potential Anti-Amyloidogenic Therapy for Type 2 Diabetes: An In Vitro Study.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Depleting prion protein using splice-switching small molecules.bioRxiv : the preprint server for biology · 2026Article
- Trends in the Engineering of Adeno-Associated Virus (AAV) for Precision Gene Delivery to the Central Nervous System (CNS).International journal of molecular sciences · 2026Review
2,226 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prions are unprecedented infectious pathogens that cause a group of invariably fatal neurodegenerative diseases by an entirely novel mechanism. Prion diseases may present as genetic, infectious, or sporadic disorders, all of which involve modification of the prion protein (PrP). Bovine spongiform encephalopathy (BSE), scrapie of sheep, and Creutzfeldt-Jakob disease (CJD) of humans are among the most notable prion diseases. Prions are transmissible particles that are devoid of nucleic acid and seem to be composed exclusively of a modified protein (PrPSc). The normal, cellular PrP (PrPC) is converted into PrPSc through a posttranslational process during which it acquires a high beta-sheet content. The species of a particular prion is encoded by the sequence of the chromosomal PrP gene of the mammals in which it last replicated. In contrast to pathogens carrying a nucleic acid genome, prions appear to encipher strain-specific properties in the tertiary structure of PrPSc. Transgenetic studies argue that PrPSc acts as a template upon which PrPC is refolded into a nascent PrPSc molecule through a process facilitated by another protein. Miniprions generated in transgenic mice expressing PrP, in which nearly half of the residues were deleted, exhibit unique biological properties and should facilitate structural studies of PrPSc. While knowledge about prions has profound implications for studies of the structural plasticity of proteins, investigations of prion diseases suggest that new strategies for the prevention and treatment of these disorders may also find application in the more common degenerative diseases.
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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.