ReviewPrion
Molecular pathogenesis of sporadic prion diseases in man.
Review in Prion. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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
29 citing papers in PubMed.
- Rapidly progressive Alzheimer's disease features distinct structures of amyloid-β.Brain : a journal of neurology · 2015Trial
- Exploring the Relationship Between Sporadic Creutzfeldt-Jakob Disease and Gut Microbiota Through a Mendelian Randomization Study.Molecular neurobiology · 2025Article
- Article
- Molecular Mechanisms Underlying Neuroinflammation Elicited by Occupational Injuries and Toxicants.International journal of molecular sciences · 2023Review
- Populations of Tau Conformers Drive Prion-like Strain Effects in Alzheimer's Disease and Related Dementias.Cells · 2022Review
- Description of the first Spanish case of Gerstmann-Sträussler-Scheinker disease with A117V variant: clinical, histopathological and biochemical characterization.Journal of neurology · 2022Article
- Role of Biomarkers for the Diagnosis of Prion Diseases: A Narrative Review.Medicina (Kaunas, Lithuania) · 2022Review
- Distinct populations of highly potent TAU seed conformers in rapidly progressing Alzheimer's disease.Science translational medicine · 2022Article
- PMCA-Based Detection of Prions in the Olfactory Mucosa of Patients With Sporadic Creutzfeldt-Jakob Disease.Frontiers in aging neuroscience · 2022Article
- Distinct conformers of amyloid beta accumulate in the neocortex of patients with rapidly progressive Alzheimer's disease.The Journal of biological chemistry · 2021Article
- Sporadic Creutzfeldt-Jakob disease: Real-Time Quaking Induced Conversion (RT-QuIC) assay represents a major diagnostic advance.European journal of histochemistry : EJH · 2021Review
- Structurally distinct external solvent-exposed domains drive replication of major human prions.PLoS pathogens · 2021Article
- The importance of ongoing international surveillance for Creutzfeldt-Jakob disease.Nature reviews. Neurology · 2021Review
- Diverse, evolving conformer populations drive distinct phenotypes in frontotemporal lobar degeneration caused by the same MAPT-P301L mutation.Acta neuropathologica · 2020Article
- Chronic wasting disease (CWD) prion strains evolve via adaptive diversification of conformers in hosts expressing prion protein polymorphisms.The Journal of biological chemistry · 2020Article
- The ecology of chronic wasting disease in wildlife.Biological reviews of the Cambridge Philosophical Society · 2020Review
- Review
- Retinal correlates of neurological disorders.Therapeutic advances in chronic disease · 2019Review
- Recent Insights on Alzheimer's Disease Originating from Yeast Models.International journal of molecular sciences · 2018Review
- Distinct prion-like strains of amyloid beta implicated in phenotypic diversity of Alzheimer's disease.Prion · 2016Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
The yeast, fungal and mammalian prions determine heritable and infectious traits that are encoded in alternative conformations of proteins. They cause lethal sporadic, familial and infectious neurodegenerative conditions in man, including Creutzfeldt-Jakob disease (CJD), Gerstmann-Sträussler-Scheinker syndrome (GSS), kuru, sporadic fatal insomnia (SFI) and likely variable protease-sensitive prionopathy (VPSPr). The most prevalent of human prion diseases is sporadic (s)CJD. Recent advances in amplification and detection of prions led to considerable optimism that early and possibly preclinical diagnosis and therapy might become a reality. Although several drugs have already been tested in small numbers of sCJD patients, there is no clear evidence of any agent's efficacy. Therefore, it remains crucial to determine the full spectrum of sCJD prion strains and the conformational features in the pathogenic human prion protein governing replication of sCJD prions. Research in this direction is essential for the rational development of diagnostic as well as therapeutic strategies. Moreover, there is growing recognition that fundamental processes involved in human prion propagation - intercellular induction of protein misfolding and seeded aggregation of misfolded host proteins - are of far wider significance. This insight leads to new avenues of research in the ever-widening spectrum of age-related human neurodegenerative diseases that are caused by protein misfolding and that pose a major challenge for healthcare.
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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.