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Attention deficit hyperactivity disorder (ADHD) is a common childhood-onset neurodevelopmental disorder. Comorbidity with other neurodevelopmental conditions, learning problems and psychiatric disorders is high and ADHD symptoms themselves, particularly inattention, can also persist into adulthood. ADHD is indexed by high levels of functional impairment and adversely affects social relationships, academic achievements and employment record. Rates of substance misuse and smoking behaviours are elevated, contributing to the physical and mental health disadvantage of those with ADHD.
Although highly heritable, ADHD is aetiologically complex whereby the coaction and interaction of inherited and non-inherited factors likely play a role in its development, maintenance and adverse consequences. Indeed, no single causal risk factor, genetic or otherwise, has been identified to date as is the case for all common, complex disorders. The evidence suggests there is contribution from both common genetic variants of small effect size and rare variants (copy number variants) of larger effect size.1 Such variants have been found to impact on similar biological pathways, interestingly including one related to nicotinic acetylcholine receptor signalling.2 ,3 There is also growing evidence that ADHD inherited risks and associated gene variants have different phenotypic effects (pleiotropy). That is, the same set of genetic risks appears to …