ReviewAnnual review of pathology2019
Cellular and Molecular Mechanisms of Prion Disease.
Review in Annual review of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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
85 citing papers in PubMed, 3 syntheses or guidelines pooled it, 159 citations in OpenAlex.
- Pooled it
- Systematic review of pharmacological management in Creutzfeldt-Jakob disease: no options so far?Arquivos de neuro-psiquiatria · 2022Pooled it
- The First Meta-Analysis of the M129V Single-Nucleotide Polymorphism (SNP) of the Prion Protein Gene (Cells · 2021Pooled it
- When copper turns killer: Decoding copper dyshomeostasis and cuproptosis in neurodegenerative pathogenesis and precision metal interventions.Neural regeneration research · 2026Article
- Cross-Omic Comparative Analysis Identifies Transcriptomic Signatures and Exploratory Gene Set-Level Signals in Sporadic Creutzfeldt-Jakob Disease.International journal of molecular sciences · 2026Article
- DL-3-n-Butylphthalide Protects Against PrPCNS neuroscience & therapeutics · 2026Article
- OPA1 Requires ATP Synthase Activity and Oligomerization to Mitigate Prion-Induced Mitochondrial Dysfunction, Oxidative Stress, and Neuronal Apoptosis.Molecular neurobiology · 2026Article
- Bovine Spongiform Encephalopathy: An Integrated Review of Prion Mechanisms, Neuroanatomy, and Control.Veterinary sciences · 2026Review
- Review
- The Landscape of Ferritin Nanocages for Neurodegenerative Diseases Treatment.International journal of nanomedicine · 2026Review
- FIS1 dependent peripheral fission exacerbates mitochondrial fragmentation and dysfunction in prion diseases.Frontiers in neuroscience · 2026Article
- Therapeutic strategies in prion disease: current evidence, translational challenges, and emerging directions.Frontiers in neuroscience · 2026Review
- A critical perspective of prion disease surveillance in Brazil.Frontiers in neuroscience · 2026Article
- Novel anti-prion compounds screening in prion-infected cell culture model combined with surface plasmon resonance analysis.Scientific reports · 2025Article
- Article
- Navigating the landscape of protein folding and proteostasis: from molecular chaperones to therapeutic innovations.Signal transduction and targeted therapy · 2025Review
- Role of cellular prion protein in mouse granulosa cells and its effects on ovarian function in knockout mice.Molecular medicine reports · 2025Article
- White-Tailed Deer Prion Protein Gene Variability Suggests Selection Against Chronic Wasting Disease in Canada's Prairies.Viruses · 2025Article
- A Drosophila model of prion disease and its metabolic changes in the brain.Animal models and experimental medicine · 2025Article
- Advances in Single-Cell Sequencing for Infectious Diseases: Progress and Perspectives.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
25 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
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Prion diseases are rapidly progressive, incurable neurodegenerative disorders caused by misfolded, aggregated proteins known as prions, which are uniquely infectious. Remarkably, these infectious proteins have been responsible for widespread disease epidemics, including kuru in humans, bovine spongiform encephalopathy in cattle, and chronic wasting disease in cervids, the latter of which has spread across North America and recently appeared in Norway and Finland. The hallmark histopathological features include widespread spongiform encephalopathy, neuronal loss, gliosis, and deposits of variably sized aggregated prion protein, ranging from small, soluble oligomers to long, thin, unbranched fibrils, depending on the disease. Here, we explore recent advances in prion disease research, from the function of the cellular prion protein to the dysfunction triggering neurotoxicity, as well as mechanisms underlying prion spread between cells. We also highlight key findings that have revealed new therapeutic targets and consider unanswered questions for future research.
Indexed as
Identifiers
What 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.