- Demontis, Ditte;
- Walters, G;
- Athanasiadis, Georgios;
- Walters, Raymond;
- Therrien, Karen;
- Nielsen, Trine;
- Farajzadeh, Leila;
- Voloudakis, Georgios;
- Bendl, Jaroslav;
- Zeng, Biau;
- Zhang, Wen;
- Grove, Jakob;
- Als, Thomas;
- Duan, Jinjie;
- Satterstrom, F;
- Bybjerg-Grauholm, Jonas;
- Bækved-Hansen, Marie;
- Gudmundsson, Olafur;
- Magnusson, Sigurdur;
- Baldursson, Gisli;
- Davidsdottir, Katrin;
- Haraldsdottir, Gyda;
- Agerbo, Esben;
- Hoffman, Gabriel;
- Dalsgaard, Søren;
- Martin, Joanna;
- Ribasés, Marta;
- Boomsma, Dorret;
- Soler Artigas, Maria;
- Roth Mota, Nina;
- Howrigan, Daniel;
- Medland, Sarah;
- Zayats, Tetyana;
- Rajagopal, Veera;
- Nordentoft, Merete;
- Mors, Ole;
- Hougaard, David;
- Mortensen, Preben;
- Daly, Mark;
- Faraone, Stephen;
- Stefansson, Hreinn;
- Roussos, Panos;
- Franke, Barbara;
- Werge, Thomas;
- Neale, Benjamin;
- Stefansson, Kari;
- Børglum, Anders
Attention-deficit hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder with a major genetic component. Here, we present a genome-wide association study meta-analysis of ADHD comprising 38,691 individuals with ADHD and 186,843 controls. We identified 27 genome-wide significant loci, highlighting 76 potential risk genes enriched among genes expressed particularly in early brain development. Overall, ADHD genetic risk was associated with several brain-specific neuronal subtypes and midbrain dopaminergic neurons. In exome-sequencing data from 17,896 individuals, we identified an increased load of rare protein-truncating variants in ADHD for a set of risk genes enriched with probable causal common variants, potentially implicating SORCS3 in ADHD by both common and rare variants. Bivariate Gaussian mixture modeling estimated that 84-98% of ADHD-influencing variants are shared with other psychiatric disorders. In addition, common-variant ADHD risk was associated with impaired complex cognition such as verbal reasoning and a range of executive functions, including attention.