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Turley, Patrick

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Turley

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Patrick

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Turley, Patrick

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2016 - 20194

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Author's Publications: search.filters.isAuthorOfPublication.0493a708-88c3-4e07-be86-4f2c6ba62432

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Now showing 1 - 4 of 4
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    Publication
    Identification of common genetic risk variants for autism spectrum disorder
    (Springer Science and Business Media LLC, 2019-02-25) Grove, Jakob; Ripke, Stephan; Als, Thomas D.; Mattheisen, Manuel; Walters, Raymond; Won, Hyejung; Pallesen, Jonatan; Agerbo, Esben; Andreassen, Ole A.; Anney, Richard; Awashti, Swapnil; Belliveau, Rich; Bettella, Francesco; Buxbaum, Joseph D.; Bybjerg-Grauholm, Jonas; Bækvad-Hansen, Marie; Cerrato, Felecia; Chambert, Kimberly; Christensen, Jane H.; Churchhouse, Claire; Dellenvall, Karin; Demontis, Ditte; De Rubeis, Silvia; Devlin, Bernie; Djurovic, Srdjan; Dumont, Ashley; Goldstein, Jacqueline; Hansen, Christine S.; Hauberg, Mads Engel; Hollegaard, Mads V.; Hope, Sigrun; Howrigan, Daniel; Huang, Hailiang; Hultman, Christina M.; Klei, Lambertus; Maller, Julian; Martin, Joanna; Martin, Alicia R.; Moran, Jennifer; Nyegaard, Mette; Nærland, Terje; Palmer, Duncan; Palotie, Aarno; Pedersen, Carsten Bøcker; Pedersen, Marianne Giørtz; Poterba, Timothy; Pourcain, Beate St; Poulsen, Jesper Buchhave; Qvist, Per; Rehnström, Karola; Reichenberg, Abraham; Reichert, Jennifer; Robinson, Elise; Roeder, Kathryn; Roussos, Panos; Saemundsen, Evald; Sandin, Sven; Satterstrom, F. Kyle; Davey Smith, George; Stefansson, Hreinn; Steinberg, Stacy; Stevens, Christine R.; Sullivan, Patrick F.; Turley, Patrick; Walters, G. Bragi; Xu, Xinyi; Stefansson, Kari; Geschwind, Daniel H.; Nordentoft, Merete; Hougaard, David M.; Werge, Thomas; Mors, Ole; Mortensen, Preben Bo; Neale, Benjamin; Daly, Mark; Børglum, Anders D.
    Autism spectrum disorder (ASD) is a highly heritable and heterogeneous group of neurodevelopmental phenotypes diagnosed in more than 1% of children. Common genetic variants contribute substantially to ASD susceptibility, but to date no individual variants have been robustly associated with ASD. With a marked sample size increase from a unique Danish population resource, we report a genome-wide association meta-analysis of 18,381 ASD cases and 27,969 controls that identifies five genome-wide significant loci. Leveraging GWAS results from three phenotypes with significantly overlapping genetic architectures (schizophrenia, major depression, and educational attainment), seven additional loci shared with other traits are identified at equally strict significance levels. Dissecting the polygenic architecture we find both quantitative and qualitative polygenic heterogeneity across ASD subtypes, in contrast to what is typically seen in other complex disorders. These results highlight biological insights, particularly relating to neuronal function and corticogenesis and establish that GWAS performed at scale will be much more productive in the near term in ASD, just as it has been in a broad range of important psychiatric and diverse medical phenotypes.
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    Publication
    Genetic associations with subjective well-being also implicate depression and neuroticism
    (Nature Publishing Group, 2016) Okbay, Aysu; Baselmans, Bart M. L.; De Neve, Jan-Emmanuel; Turley, Patrick; Nivard, Michel G.; Fontana, Mark A.; Meddens, Fleur S. W.; Linnér, Richard Karlsson; Rietveld, Cornelius A.; Derringer, Jaime; Gratten, Jacob; Lee, James J.; Liu, Jimmy Z.; de Vlaming, Ronald; Conley, Dalton C.; Smith, George Davey; Hofman, Albert; Johannesson, Magnus; Laibson, David; Medland, Sarah E.; Meyer, Michelle N.; Pickrell, Joseph; Esko, Tõnu; Krueger, Robert F.; Beauchamp, Jonathan Pierre; Koellinger, Philipp D.; Benjamin, Daniel J.; Bartels, Meike; Cesarini, David; Benjamin, Daniel; Koellinger, Philipp
    We conducted a genome-wide association study of subjective well-being (SWB) in 298,420 individuals. We also performed auxiliary analyses of depressive symptoms (“DS”; N = 161,460) and neuroticism (N = 170,910), both of which have a substantial genetic correlation with SWB (휌̂≈−0.8). We identify three SNPs associated with SWB at genome-wide significance. Two of them are significantly associated with DS in an independent sample. In our auxiliary analyses, we identify 13 additional genome-wide-significant associations: two with DS and eleven with neuroticism, including two inversion polymorphisms. Across our phenotypes, loci regulating expression in central nervous system and adrenal/pancreas tissues are enriched. The discovery of genetic loci associated with the three phenotypes we study has proven elusive; our findings illustrate the payoffs from studying them jointly.
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    Publication
    Essays in Economics and Education
    (2016-05-10) Turley, Patrick; Laibson, David; Katz, Larry; Benjamin, Daniel
    Education is a fundamental input of human capital formation. In this dissertation we explore topics related to how much and what time of human capital individuals invest in, and the long term-consequences of these investments. We begin with by measuring the degree to which financial incentives can affect a college student’s field of study. Next, we attempt to identify genetic variants associated with increased educational attainment and examine the biological systems implicated by this analysis. Last, we test for heterogeneous treatment effects of education on health across the distribution of observed health and across a genetic predictor of health. In chapter 1, we examine whether students respond to immediate financial incentives when choosing their college major. From 2006-07 to 2010-11, low-income students in technical or foreign language majors could receive up to $8,000 in SMART Grants. Since income-eligibility was determined using a strict threshold, we determine the causal impact of this grant on student major with a regression discontinuity design. Using administrative data from public universities in Texas, we determine that income-eligible students were 3.2 percentage points more likely than their ineligible peers to major in targeted fields. We measure a larger impact of 10.2 percentage points at Brigham Young University. In chapter 2 we find that, educational attainment (EA) is strongly influenced by social and other environmental factors, but genetic factors are also estimated to account for at least 20% of the variation across individuals. We report the results of a genome-wide association study (GWAS) for EA that extends our earlier discovery sample of 101,069 individuals to 293,723 individuals, and a replication in an independent sample of 111,349 individuals from the UK Biobank. We now identify 74 genome-wide significant loci associated with number of years of schooling completed. Single-nucleotide polymorphisms (SNPs) associated with educational attainment are disproportionately found in genomic regions regulating gene expression in the fetal brain. Candidate genes are preferentially expressed in neural tissue, especially during the prenatal period, and enriched for biological pathways involved in neural development. Our findings demonstrate that, even for a behavioral phenotype that is mostly environmentally determined, a well-powered GWAS identifies replicable associated genetic variants that suggest biologically relevant pathways. Because EA is measured in large numbers of individuals, it will continue to be useful as a proxy phenotype in efforts to characterize the genetic influences of related phenotypes, including cognition and neuropsychiatric disease. In 1972, the mandatory minimum age at which a student could drop out of school in England and Wales was raised from 15 to 16, constraining roughly 15 percent of the student population. In chapter 3, we exploit this discontinuous increase in educational attainment to estimate the impact of education on body mass index (BMI) and diabetes approximately 40 years later. While previous literature found no significant effect of education on health, they were not able to investigate whether these effects vary along the distribution of health outcomes. We are able to detect large effects on BMI in the upper quantiles of observed BMI, as large as 2 BMI points at the 90th percentile of BMI, from a baseline of 35.6. Using a genetic predictor of BMI, we also find that those with higher genetic risk of obesity see smaller reductions in BMI as a result of the increase in compulsory schooling while large reductions are seen in those with low genetic risk. Taken together our results point to the importance of considering heterogeneity when estimating the impacts of education on health.
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    Publication
    Genome-wide study of risk tolerance and risky behaviors reveals shared genetic influences
    (Springer-Nature, 2017) Karlsson Linner, Richard; Biroli, Pietro; Kong, Edward; Meddens, S. Fleur W.; Wedow, Robbee; Fontana, Mark Alan; Lebreton, Mael; Abdellaoui, Abdel; Hammerschlag, Anke R.; Nivard, Michel G.; Okbay, Aysu; Rietveld, Cornelius A.; Timshel, Pascal N.; Tino, Stephen P.; Trzaskowski, Maciej; de Vlaming, Ronald; Zund, Christian L.; Bao, Yanchun; Buzdugan, Laura; Caplin, Ann H.; Chen, Chia-Yen; Eibich, Peter; Fontanillas, Pierre; Joshi, Peter K.; Karhunen, Ville; Kleinman, Aaron; Levin, Remy Z.; Lill, Christina M.; Meddens, Gerardus A.; Muntane, Gerard; Sanchez-Roige, Sandra; Gonzalez, Juan Ramon; van Rooij, Frank J.; Taskesen, Erdogan; Wu, Yang; Zhang, Futao; Auton, Adam; Boardman, Jason D.; Clark, David W.; Conlin, Andrew; Dolan, Conor C.; Fischbacher, Urs; Groenen, Patrick J. F.; Harris, Kathleen Mullan; Hasler, Gregor; Hofman, Albert; Ikram, Mohammad A.; Jain, Sonia; Karlsson, Robert; MacKillop, James; Mannikko, Minna; Morcillo-Suarez, Carlos; McQueen, Matthew B.; Schmidt, Klaus M.; Smart, Melissa C.; Sutter, Matthias; Thurik, A. Roy; Uitterlinden, Andre G.; White, Jon; de Wit, Harriet; Yang, Jian; Bertram, Lars; Boomsma, Dorret; Esko, Tonu; Fehr, Ernst; Hinds, David A.; Johannesson, Magnus; Kumari, Meena; Laibson, David; Magnusson, Patrik K. E.; Meyer, Michelle N.; Navarro, Arcadi; Palmer, Abraham A.; Pers, Tune H.; Posthuma, Danielle; Schunk, Daniel; Stein, Murray B.; Svento, Rauli; Tiemeier, Henning; Timmers, Paul R. H. J.; Turley, Patrick; Ursano, Robert J.; Wagner, Gert G.; Wilson, James F.; Gratten, Jacob; Lee, James J.; Cesarini, David; Benjamin, Daniel J.; Koellinger, Philipp D.; Beauchamp, Jonathan P.
    Risk tolerance is an important variable in the behavioral and social sciences and one of the most studied phenotypes in social science genetics, but few genetic variants have so far been found to robustly associate with it or with risky behaviors.