ReviewVirulence2013
Infectious particles, stress, and induced prion amyloids: a unifying perspective.
Review in Virulence, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Reduced Expression of Prion Protein With Increased Interferon-β Fail to Limit Creutzfeldt-Jakob Disease Agent Replication in Differentiating Neuronal Cells.Frontiers in physiology · 2022Article
- Linking Oxidative Stress and Proteinopathy in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Retinal Microvasculature and Conjunctival Vessel Alterations in Patients With Systemic Lupus Erythematosus-An Optical Coherence Tomography Angiography Study.Frontiers in medicine · 2021Article
- Elucidating Critical Proteinopathic Mechanisms and Potential Drug Targets in Neurodegeneration.Cellular and molecular neurobiology · 2020Review
- Prion protein PrP nucleic acid binding and mobilization implicates retroelements as the replicative component of transmissible spongiform encephalopathy.Archives of virology · 2020Review
- Implications of peptide assemblies in amyloid diseases.Chemical Society reviews · 2017Review
- A prokaryotic viral sequence is expressed and conserved in mammalian brain.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- The Biological Function of the Prion Protein: A Cell Surface Scaffold of Signaling Modules.Frontiers in molecular neuroscience · 2017Article
- Proteomic analysis of host brain components that bind to infectious particles in Creutzfeldt-Jakob disease.Proteomics · 2015Article
- Rapid chemical decontamination of infectious CJD and scrapie particles parallels treatments known to disrupt microbes and biofilms.Virulence · 2015Article
- Synthetic scrapie infectivity: interaction between recombinant PrP and scrapie brain-derived RNA.Virulence · 2015Article
- Highly infectious CJD particles lack prion protein but contain many viral-linked peptides by LC-MS/MS.Journal of cellular biochemistry · 2014Article
- Susceptibility of GT1-7 cells to mouse-passaged field scrapie isolates with a long incubation.Prion · 2014Article
- Alzheimer's disease and the microbiome.Frontiers in cellular neuroscience · 2013Article
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
Transmissible encephalopathies (TSEs) are believed by many to arise by spontaneous conversion of host prion protein (PrP) into an infectious amyloid (PrP-res, PrP (Sc) ) without nucleic acid. Many TSE agents reside in the environment, with infection controlled by public health measures. These include the disappearance of kuru with the cessation of ritual cannibalism, the dramatic reduction of epidemic bovine encephalopathy (BSE) by removal of contaminated feed, and the lack of endemic scrapie in geographically isolated Australian sheep with susceptible PrP genotypes. While prion protein modeling has engendered an intense focus on common types of protein misfolding and amyloid formation in diverse organisms and diseases, the biological characteristics of infectious TSE agents, and their recognition by the host as foreign entities, raises several fundamental new directions for fruitful investigation such as: (1) unrecognized microbial agents in the environmental metagenome that may cause latent neurodegenerative disease, (2) the evolutionary social and protective functions of different amyloid proteins in diverse organisms from bacteria to mammals, and (3) amyloid formation as a beneficial innate immune response to stress (infectious and non-infectious). This innate process however, once initiated, can become unstoppable in accelerated neuronal aging.
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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.