Despite the pervasive overlap, the number of shared and unique ‘causal’ variants varied across phenotypic pairs, sometimes revealing the presence of strongly correlated shared variants despite moderate genome-wide genetic correlation. This pattern was most evident between ADHD and MD, a finding supported by LAVA. This suggests that, although a large proportion of MD associated variants are not associated with ADHD, those which are shared have highly similar effects. This mirrors recent findings from a genomic structural equation modelling (Genomic SEM) approach that clustered MD with neurodevelopmental disorders including ADHD.8 This may indicate distinct clinical sub-groups with higher rates of co-morbidity, or shared involvement of specific molecular mechanisms with similar effects on both disorders. Further investigation of the shared genetic architecture of ADHD and MD may prove fruitful for the identification of underlying biological mechanisms and new treatment targets.42–44
