ReviewBrain pathology (Zurich, Switzerland)1998
The prion diseases.
Review in Brain pathology (Zurich, Switzerland), 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 3 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
155 citing papers in PubMed, 3 syntheses or guidelines pooled it, 401 citations in OpenAlex.
- Systematic Review of Clinical and Pathophysiological Features of Genetic Creutzfeldt-Jakob Disease Caused by a Val-to-Ile Mutation at Codon 180 in the Prion Protein Gene.International journal of molecular sciences · 2022Pooled it
- The First Meta-Analysis of the M129V Single-Nucleotide Polymorphism (SNP) of the Prion Protein Gene (Cells · 2021Pooled it
- 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
- Life at the interface: Byron Caughey's search for prion disease inhibitors through chemistry, structure, and cell physiology.Acta neuropathologica · 2026Review
- Prnp Deletion Mitigates Muscle Fiber Type-Specific Sarcopenia Induced by Prion Infection in Mice.Immunity, inflammation and disease · 2026Article
- A fixed brain seeded amplification assay to complement neuropathological prion disease diagnosis.Journal of neuropathology and experimental neurology · 2026Article
- Therapeutic effects of adipose-derived mesenchymal stem cells combined with glymphatic system activation in prion disease.Molecular neurodegeneration · 2025Article
- Delayed progression of prion disease in mice by polyarginine-facilitated prevention of PrPNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Biological characteristics and transcriptomic profile of adipose-derived mesenchymal stem cells isolated from prion-infected murine model.Stem cell research & therapy · 2025Article
- Microbes Saving Lives and Reducing Suffering.Microbial biotechnology · 2025Article
- Prion Disease Diagnostic Biomarker Utility in Pre-symptomatic Disease.Sub-cellular biochemistry · 2025Review
- Article
- Protective role of cytosolic prion protein against virus infection in prion-infected cells.Journal of virology · 2024Article
- Screening of Anti-Prion Compounds Using the Protein Misfolding Cyclic Amplification Technology.Biomolecules · 2024Article
- Novel Single-Nucleotide Polymorphisms (SNPs) and Genetic Studies of the Shadow of Prion Protein (Animals : an open access journal from MDPI · 2024Article
- Transmission of Norwegian reindeer CWD to sheep by intracerebral inoculation results in an unusual phenotype and prion distribution.Veterinary research · 2024Article
- Different reactive profiles of calmodulin in the CSF samples of Chinese patients of four types of genetic prion diseases.Frontiers in molecular neuroscience · 2024Article
- Article
- Synthesis and anti-prion aggregation activity of acylthiosemicarbazide analogues.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- Article
95 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
Abstract
The human prion diseases are fatal neurodegenerative maladies that may present as sporadic, genetic, or infectious illnesses. The sporadic form is called Creutzfeldt-Jakob disease (CJD) while the inherited disorders are called familial (f) CJD, Gerstmann-Straussler-Scheinker (GSS) disease and fatal familial insomnia (FFI). 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. In fCJD, GSS, and FFI, mutations in the PrP gene located on the short arm of chromosome 20 are the cause of disease. Considerable evidence argues that the prion diseases are disorders of protein conformation.
Indexed as
Identifiers
9669700PMC8098303W2164123708What OpenQuestion holds
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.