ArticleJournal of neurology2012
Codon 200 mutation of the prion gene: genotype-phenotype correlations.
Article in Journal of neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Movement Disorders in Prionopathies: A Systematic Review.Tremor and other hyperkinetic movements (New York, N.Y.) · 2019Pooled it
- A Practice Framework for Genetic Testing in Asymptomatic Relatives of Patients With Creutzfeldt-Jakob Disease: Experience and Insights From Israel.European journal of neurology · 2026Article
- Lacritin and other autophagy associated proteins in ocular surface health.Experimental eye research · 2016Review
- Prion diseases: immunotargets and therapy.ImmunoTargets and therapy · 2016Review
- Biological network inferences for a protection mechanism against familial Creutzfeldt-Jakob disease with E200K pathogenic mutation.BMC medical genomics · 2014Article
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic mutations as a cause of prion diseases are rare. We describe a large family with multiple affected members with the codon E200K prion mutation. To improve understanding of the genotype-phenotype correlations of prion gene mutations, clinical, genetic and neuropathological data were obtained from family members over 15 years. Six patients with the codon E200K mutation and 2 patients without the codon 200 mutation from this family were followed. The 6 patients with the codon 200 mutation had a mean age onset of 58.83 years (SD 7.2; lower 95 % CI 51.0; upper 95 % CI 66.4). The most common symptoms at onset were memory loss, walking difficulties and hallucinations. The most frequent neurological phenomena were a rapidly progressive dementia, eye movement abnormalities and ataxia. The mean duration of onset of symptoms to death was 3.9 months (SD 1.1; lower 95 % CI 2.8; upper 95 % CI 5.1). Two male patients developed neurodegenerative disorders unrelated to the prion codon 200 mutation: progressive supranuclear palsy and olivopontocerebellar degeneration. Their mean survival was 96 months (SD 33.9; p < 0.0001). Individuals from families with the prion codon 200 mutation may have a rapidly progressive dementia. Members of families with inherited prion mutations may be at risk of other neurodegenerative disorders unrelated to the prion mutation.
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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.