In summary, we identified new ADHD risk loci, highlighted candidate causal genes, and implicated genes expressed in frontal cortex and several brain specific neuronal subtypes in ADHD. Our analyses revealed ADHD to be highly polygenic, influenced by thousands of variants, of which the vast majority also influence other psychiatric disorders with concordant or discordant effects. Additionally, we demonstrated that common variant ADHD risk has an impairing impact on a range of executive functions. Overall, the results advance our understanding of the underlying biology of ADHD and reveal novel aspects of ADHD’s polygenic architecture, its relationship with other phenotypes, and its impact on cognitive domains.
