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Genome‐wide association analysis of actigraphic sleep phenotypes in the LIFE Adult Study
Author(s) -
Spada Janek,
Scholz Markus,
Kirsten Holger,
Hensch Tilman,
Horn Katrin,
Jawinski Philippe,
Ulke Christine,
Burkhardt Ralph,
Wirkner Kerstin,
Loeffler Markus,
Hegerl Ulrich,
Sander Christian
Publication year - 2016
Publication title -
journal of sleep research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.297
H-Index - 117
eISSN - 1365-2869
pISSN - 0962-1105
DOI - 10.1111/jsr.12421
Subject(s) - genome wide association study , heritability , snp , phenotype , sleep (system call) , imputation (statistics) , genetic association , actigraphy , single nucleotide polymorphism , sleep quality , sleep onset latency , circadian rhythm , biology , candidate gene , genetics , psychology , medicine , insomnia , gene , genotype , neuroscience , psychiatry , computer science , missing data , operating system , machine learning
Summary The genetic basis of sleep is still poorly understood. Despite the moderate to high heritability of sleep‐related phenotypes, known genetic variants explain only a small proportion of the phenotypical variance. However, most previous studies were based solely upon self‐report measures. The present study aimed to conduct the first genome‐wide association (GWA) of actigraphic sleep phenotypes. The analyses included 956 middle‐ to older‐aged subjects (40–79 years) from the LIFE Adult Study. The SenseWear Pro 3 Armband was used to collect 11 actigraphic parameters of night‐ and daytime sleep and three parameters of rest (lying down). The parameters comprised measures of sleep timing, quantity and quality. A total of 7 141 204 single nucleotide polymorphisms ( SNP s) were analysed after imputation and quality control. We identified several variants below the significance threshold of P ≤ 5× 10 −8 (not corrected for analysis of multiple traits). The most significant was a hit near UFL 1 associated with sleep efficiency on weekdays ( P = 1.39 × 10 −8 ). Further SNP s were close to significance, including an association between sleep latency and a variant in CSNK 2A1 ( P = 8.20 × 10 −8 ), a gene known to be involved in the regulation of circadian rhythm. In summary, our GWAS identified novel candidate genes with biological plausibility being promising candidates for replication and further follow‐up studies.