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Attention-Deficit Hyperactivity Disorder (ADHD) is one of the most common and heritable childhood onset psychiatric conditions. The clinical phenotype is multidimensional with main symptoms being inattention and/or hyperactivity/impulsivity. As ADHD persists into adulthood (in up to ~80% of cases), some symptoms become more pronounced than others. Furthermore, the various aggregates of dimensions are associated with different clinical features (e.g. co-morbidities) and treatment outcomes of ADHD. So far, the biology behind such symptomatology of ADHD is far from understood. In this study, we aimed to explore the genetics of ADHD dimensions in children and their correlation with neuropsychiatric phenotypes in adulthood. The childhood sample consisted of 11,784 children from (1) Australia (N=4,000), (2) Canada (N=4,339) and (3) Norway (The Norwegian Mother Child Cohort (MoBa), N=3,445). ADHD dimensions were measured by the Strengths and Weaknesses of ADHD and Normal Behavior (SWAN) rating scale in Australia and Canada, and by Swanson, Nolan and Pelham, Teacher and Parent Rating Scale (SNAP) in Norway. The genetic similarity of SWAN and SNAP measures was assessed by LD regression. We also examined how genetic risk for ADHD symptoms correlated with neuropsychiatric phenotypes in adulthood, including schizophrenia, major depression disorder, bipolar disorder, Alzheimer's disorder, subjective well-being, neuroticism and educational attainment. Overall, our preliminary results (N=3,445, SNAP data) suggest that the genetics of hyperactivity/impulsivity dimension in childhood show higher correlation with genetics of neuropsychiatric phenotypes in adulthood than that of childhood inattention, with strong contrasts between genetic correlations of hyperactivity/impulsivity and inattention with schizophrenia (h2=-0.115 and 0.0037), depressive symptoms (h2=0.483 and 0.278), subjective well-being (h2=-0.564 and -0.369), anxiety (h2=0.307 and 0.188) and Alzheimer's disease (h2=0.280 and 0.076). We will present the results from the full sample(N=11,784). Further exploration of how ADHD dimensions in childhood relate/lead to neuropsychiatric pathology in adulthood will aid our understanding of biological processes underlying ADHD symptomatology and, potentially, lead to better diagnosis, treatment and prevention options for ADHD. [ABSTRACT FROM AUTHOR]