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Abstract Details

Genetic Correlation and Overlap Between Sleep Traits and Cerebral Small Vessel Disease
Cerebrovascular Disease and Interventional Neurology
Cerebrovascular Disease and Interventional Neurology Posters (7:00 AM-5:00 PM)
188

To investigate the genetic correlation and overlap between sleep traits, stroke, and manifestations of CSVD.
Several epidemiologic studies have emerged linking sleep phenotypes with stroke and its subtypes. However, the extent to which these traits are genetically correlated, and the degree to which these correlations persist across cerebral small vessel disease (CSVD) phenotypes, remains unknown.
We leveraged data from large genome-wide association studies (GWAS) of two sleep phenotypes (short sleep, insomnia) and four stroke/CSVD phenotypes [ischemic stroke (IS), small vessel stroke (SVS), intracerebral hemorrhage (ICH), white matter hyperintensities (WMH)]. We assessed the genetic correlation between the sleep and the CSVD phenotypes using linkage disequilibrium score regression (LDSC) and polygenic risk score (PRS) analyses. False discovery rate (FDR) was used to correct for multiple hypothesis testing; significant associations before FDR correction were considered of nominal significance.
Using LDSC, we found significant genetic correlations between short sleep and IS and SVS (rg=0.19, FDR-p<0.001 and rg=0.31, FDR-p=0.02 respectively), as well as a nominal association between short sleep and WMH (rg=0.11, p=0.05). We also found significant genetic correlations between insomnia and IS and SVS (rg=0.12, FDR-p=0.02 and rg=0.33, FDR-p=0.02 respectively). Our PRS analyses extended these findings, identifying a genetic overlap between insomnia and ICH (OR=1.09 per 1 SD increase; 95% CI=1.02-1.17; FDR-p=0.03) as well as a nominal association between insomnia and SVS (OR=1.05 per 1 SD increase; 95% CI=1.00-1.09, p=0.05).

We identified and quantified genome-wide genetic correlations between short sleep and insomnia with stroke, and specifically CSVD phenotypes. Further analyses are needed to uncover potential local genetic correlations and pleiotropic loci affecting these traits, as well as the directionality and causality of these correlations.
Authors/Disclosures
Evangelos Pavlos Myserlis, MD (Department of Neurology)
PRESENTER 		The institution of Dr. Myserlis has received research support from Â鶹´«Ã½Ó³»­. Dr. Myserlis has received personal compensation in the range of $500-$4,999 for serving as a Â鶹´«Ã½Ó³»­ Resident Scholarship to the Annual Meeting Recipient with Â鶹´«Ã½Ó³»­.
Jonathan Rosand, MD (Massachusetts General Hospital) Dr. Rosand has received personal compensation for serving as an employee of Massachusetts General Hospital. Dr. Rosand has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Eli Lilly and Co. Dr. Rosand has received personal compensation in the range of $0-$499 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Elsevier. The institution of Dr. Rosand has received research support from NIH. The institution of Dr. Rosand has received research support from American Heart Association. Dr. Rosand has received personal compensation in the range of $0-$499 for serving as a Peer reviewer with National Institutes of Health. Dr. Rosand has a non-compensated relationship as a Trustee with Columbia University that is relevant to Â鶹´«Ã½Ó³»­ interests or activities.
Christopher D. Anderson, MD, PhD, FÂ鶹´«Ã½Ó³»­ (Brigham and Women's Hospital) The institution of Dr. Anderson has received research support from Bayer AG. The institution of Dr. Anderson has received research support from American Heart Association. The institution of Dr. Anderson has received research support from National Institutes of Health. An immediate family member of Dr. Anderson has received publishing royalties from a publication relating to health care.