ArticleNeuropathology and applied neurobiology2021
Met
Article in Neuropathology and applied neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 8 citations in OpenAlex.
- 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
- Limited transmission of cervid prions to nonhuman primates provides insights into the zoonotic potential of chronic wasting disease.Science advances · 2026Article
- Strain-Dependent Susceptibility to Prion Infection Encoded by Arg171 and Lys176 Sheep Prion Protein Polymorphic Variants.The Journal of infectious diseases · 2025Article
- A structural basis for prion strain diversity.Nature chemical biology · 2023Article
- Review on PRNP genetics and susceptibility to chronic wasting disease of Cervidae.Veterinary research · 2021Review
- MetNeuropathology and applied neurobiology · 2021Article
- Insight into molecular mechanisms of resistance against prion strains.Nature reviews. Neurology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThe amino acid sequence of prion protein (PrP) is a key determinant in the transmissibility of prion diseases. While PrP sequence is highly conserved among mammalian species, minor changes in the PrP amino acid sequence may confer alterations in the transmissibility of prion diseases. Classical bovine spongiform encephalopathy (C-BSE) is the only zoonotic prion strain reported to date causing variant Creutzfeldt-Jacob disease (vCJD) in humans, although experimental transmission points to atypical L-BSE and some classical scrapie isolates as also zoonotic. The precise molecular elements in the human PrP sequence that limit the transmissibility of prion strains such as sheep/goat scrapie or cervid chronic wasting disease (CWD) are not well known.
methodsThe transmissibility of a panel of diverse prions from different species was compared in transgenic mice expressing either wild-type human PrP
resultsVDQ-HuTg372 mice were more susceptible to prions than MDE-HuTg340 mice in a strain-dependent manner.
conclusionsMet
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.