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• W2911466821 abstract "Background: Cerebral white matter hyperintensities (WMH) on MRI are typical markers of small vessel disease and strong radiological correlates of stroke and age-related cognitive decline. Despite a recognized high heritability, the molecular basis of WMH has not been fully characterized. In particular, the contribution of epigenetic modifications, such as DNA methylation, has not been explored. Methods: We conducted a meta-analysis of epigenome-wide association studies of WMH burden in up to 5777 elderly participants of European and African ancestry from 9 population-based cohorts using blood-derived DNA methylation measured on the Infinium HumanMethylation450 BeadChip. Cohort-specific associations between burden of WMH and DNA methylation beta values were estimated using linear mixed-effect models and combined in a sample-size weighted fixed-effect meta-analysis. In addition, we used two different approaches to identify differentially methylated regions (DMRs), which may be more informative than individual loci. Bonferroni correction and False Discovery Rates were used to account for the multiple tests. Results: Single-site analyses identified a CpG site within the CLDN5 gene significantly associated with WMH (P= 2.3x10 -7 ). Claudin-5 is an endothelial-specific component in the brain vasculature and regulates blood brain barrier permeability. Region-based analyses, which leverage the correlations between nearby CpG sites identified several DMRs significantly associated with WMH burden including: PRMT1, BTBD17, and IFITM10 (P=1.4x10 -10 , 2.3x10 -8 , and 3.6x10 -7 , respectively). PRMT1 encodes the Protein Arginine N-methylase 1, which methylates histones in genes involved in glioblastomagenesis. Mice lacking this gene are characterized by severe defects in oligodendrocyte maturation processes. The function of BTBD17 and IFITM10 is not characterized but both are expressed in the brain and exhibit changes in expression in response to viral infection. Conclusions: Consistent with our previously reported genetic association studies, this genome-wide DNA methylation analysis supports a role of genes involved in glial cell function in WMH etiology. It also suggests a novel role of genes involved in viral response." @default.
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• W2911466821 date "2019-02-01" @default.
• W2911466821 modified "2023-10-13" @default.
• W2911466821 title "Abstract WP216: Epigenome-Wide Association Study of Cerebral White Matter Hyperintensities" @default.
• W2911466821 doi "https://doi.org/10.1161/str.50.suppl_1.wp216" @default.
• W2911466821 hasPublicationYear "2019" @default.
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