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Demontis, Ditte; Rajagopal, Veera Manikandan; Thorgeirsson, Thorgeir E; Als, Thomas D; Grove, Jakob; Leppälä, Kalle; Gudbjartsson, Daniel F; Pallesen, Jonatan; Hjorthøj, Carsten; Reginsson, Gunnar W; Tyrfingsson, Thorarinn; Runarsdottir, Valgerdur; Qvist, Per; Christensen, Jane Hvarregaard; Bybjerg-Grauholm, Jonas; Bækvad-Hansen, Marie; Huckins, Laura M; Stahl, Eli A; Timmermann, Allan; Agerbo, Esben; Hougaard, David M; Werge, Thomas; Mors, Ole; Mortensen, Preben Bo; Nordentoft, Merete; Daly, Mark J; Stefansson, Hreinn; Stefansson, Kari; Nyegaard, Mette; Børglum, Anders D
Nature neuroscience, 07/2019, Letnik: 22, Številka: 7Journal Article
Cannabis is the most frequently used illicit psychoactive substance worldwide; around one in ten users become dependent. The risk for cannabis use disorder (CUD) has a strong genetic component, with twin heritability estimates ranging from 51 to 70%. Here we performed a genome-wide association study of CUD in 2,387 cases and 48,985 controls, followed by replication in 5,501 cases and 301,041 controls. We report a genome-wide significant risk locus for CUD (P = 9.31 × 10 ) that replicates in an independent population (P = 3.27 × 10 , P = 9.09 × 10 ). The index variant (rs56372821) is a strong expression quantitative trait locus for cholinergic receptor nicotinic α2 subunit (CHRNA2); analyses of the genetically regulated gene expression identified a significant association of CHRNA2 expression with CUD in brain tissue. At the polygenic level, analyses revealed a significant decrease in the risk of CUD with increased load of variants associated with cognitive performance. The results provide biological insights and inform on the genetic architecture of CUD.
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in: SICRIS
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