Jacqueline M Lane Jingjing Liang, Irma Vlasac Simon Anderson David Bechtold Jack Bowden Richard Emsley Shubhroz Gill Max Little Annemarie Luik Andrew Loudon Frank Scheer Shaun Purcell Simon Kyle Deborah Lawlor Xiaofeng Zhu Susan Redline David Ray Martin Rutter & Richa Saxena G A A I A J L M D A W K Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits Journal Article In: Nature Genetics, 2016. Abstract | Links | BibTeX | Tags: 6818, behavioural genetics, featured, GWAS @article{JacquelineMLane2016,
title = {Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits},
author = {Jacqueline M Lane, Jingjing Liang, Irma Vlasac, Simon G Anderson, David A Bechtold, Jack Bowden, Richard Emsley, Shubhroz Gill, Max A Little, Annemarie I Luik, Andrew Loudon, Frank A J L Scheer, Shaun M Purcell, Simon D Kyle, Deborah A Lawlor, Xiaofeng Zhu, Susan Redline, David W Ray, Martin K Rutter & Richa Saxena},
url = {http://www.nature.com/ng/journal/vaop/ncurrent/full/ng.3749.html},
year = {2016},
date = {2016-12-19},
journal = {Nature Genetics},
abstract = {Chronic sleep disturbances, associated with cardiometabolic diseases, psychiatric disorders and all-cause mortality1, 2, affect 25–30% of adults worldwide3. Although environmental factors contribute substantially to self-reported habitual sleep duration and disruption, these traits are heritable4, 5, 6, 7, 8, 9 and identification of the genes involved should improve understanding of sleep, mechanisms linking sleep to disease and development of new therapies. We report single- and multiple-trait genome-wide association analyses of self-reported sleep duration, insomnia symptoms and excessive daytime sleepiness in the UK Biobank (n = 112,586). We discover loci associated with insomnia symptoms (near MEIS1, TMEM132E, CYCL1 and TGFBI in females and WDR27 in males), excessive daytime sleepiness (near AR–OPHN1) and a composite sleep trait (near PATJ (INADL) and HCRTR2) and replicate a locus associated with sleep duration (at PAX8). We also observe genetic correlation between longer sleep duration and schizophrenia risk (rg = 0.29, P = 1.90 × 10−13) and between increased levels of excessive daytime sleepiness and increased measures for adiposity traits (body mass index (BMI): rg = 0.20, P = 3.12 × 10−9; waist circumference: rg = 0.20, P = 2.12 × 10−7).},
keywords = {6818, behavioural genetics, featured, GWAS},
pubstate = {published},
tppubtype = {article}
}
Chronic sleep disturbances, associated with cardiometabolic diseases, psychiatric disorders and all-cause mortality1, 2, affect 25–30% of adults worldwide3. Although environmental factors contribute substantially to self-reported habitual sleep duration and disruption, these traits are heritable4, 5, 6, 7, 8, 9 and identification of the genes involved should improve understanding of sleep, mechanisms linking sleep to disease and development of new therapies. We report single- and multiple-trait genome-wide association analyses of self-reported sleep duration, insomnia symptoms and excessive daytime sleepiness in the UK Biobank (n = 112,586). We discover loci associated with insomnia symptoms (near MEIS1, TMEM132E, CYCL1 and TGFBI in females and WDR27 in males), excessive daytime sleepiness (near AR–OPHN1) and a composite sleep trait (near PATJ (INADL) and HCRTR2) and replicate a locus associated with sleep duration (at PAX8). We also observe genetic correlation between longer sleep duration and schizophrenia risk (rg = 0.29, P = 1.90 × 10−13) and between increased levels of excessive daytime sleepiness and increased measures for adiposity traits (body mass index (BMI): rg = 0.20, P = 3.12 × 10−9; waist circumference: rg = 0.20, P = 2.12 × 10−7). |
Lane Jacqueline M. Liang, Jingjing Vlasac Irma Anderson Simon Bechtold David Bowden Jack Emsley Richard Gill Shubhroz Little Max Luik Annemarie Loudon Andrew Scheer Frank Purcell Shaun Kyle Simon Lawlor Deborah Zhu Xiaofeng Redline Susan Ray David Rutter Martin Saxena Richa G A A I A J L M D A W K Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits Journal Article In: Nature Genetics, 2016. Abstract | Links | BibTeX | Tags: behavioural genetics, GWAS @article{LaneJM2016,
title = {Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits},
author = {Lane, Jacqueline M.
Liang, Jingjing
Vlasac, Irma
Anderson, Simon G.
Bechtold, David A.
Bowden, Jack
Emsley, Richard
Gill, Shubhroz
Little, Max A.
Luik, Annemarie I.
Loudon, Andrew
Scheer, Frank A. J. L.
Purcell, Shaun M.
Kyle, Simon D.
Lawlor, Deborah A.
Zhu, Xiaofeng
Redline, Susan
Ray, David W.
Rutter, Martin K.
Saxena, Richa},
url = {http://www.nature.com/ng/journal/vaop/ncurrent/full/ng.3749.html},
year = {2016},
date = {2016-12-19},
journal = {Nature Genetics},
abstract = {Chronic sleep disturbances, associated with cardiometabolic diseases, psychiatric disorders and all-cause mortality1, 2, affect 25–30% of adults worldwide3. Although environmental factors contribute substantially to self-reported habitual sleep duration and disruption, these traits are heritable4, 5, 6, 7, 8, 9 and identification of the genes involved should improve understanding of sleep, mechanisms linking sleep to disease and development of new therapies. We report single- and multiple-trait genome-wide association analyses of self-reported sleep duration, insomnia symptoms and excessive daytime sleepiness in the UK Biobank (n = 112,586). We discover loci associated with insomnia symptoms (near MEIS1, TMEM132E, CYCL1 and TGFBI in females and WDR27 in males), excessive daytime sleepiness (near AR–OPHN1) and a composite sleep trait (near PATJ (INADL) and HCRTR2) and replicate a locus associated with sleep duration (at PAX8). We also observe genetic correlation between longer sleep duration and schizophrenia risk (rg = 0.29, P = 1.90 × 10−13) and between increased levels of excessive daytime sleepiness and increased measures for adiposity traits (body mass index (BMI): rg = 0.20, P = 3.12 × 10−9; waist circumference: rg = 0.20, P = 2.12 × 10−7).},
keywords = {behavioural genetics, GWAS},
pubstate = {published},
tppubtype = {article}
}
Chronic sleep disturbances, associated with cardiometabolic diseases, psychiatric disorders and all-cause mortality1, 2, affect 25–30% of adults worldwide3. Although environmental factors contribute substantially to self-reported habitual sleep duration and disruption, these traits are heritable4, 5, 6, 7, 8, 9 and identification of the genes involved should improve understanding of sleep, mechanisms linking sleep to disease and development of new therapies. We report single- and multiple-trait genome-wide association analyses of self-reported sleep duration, insomnia symptoms and excessive daytime sleepiness in the UK Biobank (n = 112,586). We discover loci associated with insomnia symptoms (near MEIS1, TMEM132E, CYCL1 and TGFBI in females and WDR27 in males), excessive daytime sleepiness (near AR–OPHN1) and a composite sleep trait (near PATJ (INADL) and HCRTR2) and replicate a locus associated with sleep duration (at PAX8). We also observe genetic correlation between longer sleep duration and schizophrenia risk (rg = 0.29, P = 1.90 × 10−13) and between increased levels of excessive daytime sleepiness and increased measures for adiposity traits (body mass index (BMI): rg = 0.20, P = 3.12 × 10−9; waist circumference: rg = 0.20, P = 2.12 × 10−7). |
