ArticleStroke2020
Replication of Top Loci From COL4A1/2 Associated With White Matter Hyperintensity Burden in Patients With Ischemic Stroke.
Article in Stroke, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- The Magic and Mystery of TRIM65 in Diseases.Current medicinal chemistry · 2025Review
- Pathophysiology of cerebral small vessel disease: a journey through recent discoveries.The Journal of clinical investigation · 2024Review
- Leukoaraiosis: Epidemiology, Imaging, Risk Factors, and Management of Age-Related Cerebral White Matter Hyperintensities.Journal of stroke · 2024Review
- Dissecting Polygenic Etiology of Ischemic Stroke in the Era of Precision Medicine.Journal of clinical medicine · 2022Review
- Genetics of common cerebral small vessel disease.Nature reviews. Neurology · 2022Review
- Rare and Common Variants inFrontiers in neurology · 2022Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
background and purposeThe purpose of this study was to replicate the top loci associated with white matter hyperintensity (WMH) phenotypes identified by large genome-wide association studies and the loci identified from the previous candidate gene studies.
methodsA total of 946 Geisinger MyCode patients with acute ischemic stroke with validated European ancestry and magnetic resonance imaging data were included in this study. Log-transformed WMH volume, as a quantitative trait, was calculated by a fully automated quantification process. The genome-wide association studies was carried out by a linear mixed regression model (GEMMA). A candidate-single nucleotide polymorphism analysis by including known single nucleotide polymorphisms, reported from a meta-analysis and several large GWAS for WMH, was conducted in all cases and binary converted extreme cases.
resultsNo genome-wide significantly associated variants were identified. In a candidate-single nucleotide polymorphism study, rs9515201 (
conclusionsReplication of COL4A1/2 associated with WMH reassures that the genetic risk factors for monogenic and polygenic ischemic stroke are shared at gene level.
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Registered trials
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