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However, prior studies have not directly investigated the role in which white matter properties within the fronto\u2010basal\u2010ganglia circuit may play in the development of inhibitory control deficits in this group. Combining recent advancements in brain\u2010behavioural modelling, we mapped the development of stop\u2010signal task (SST) performance and fronto\u2010basal\u2010ganglia maturation in a longitudinal sample of children aged 9\u201314 with and without ADHD. In a large sample of 135 ADHD and 138 non\u2010ADHD children, we found that the ADHD group had poorer inhibitory control (i.e., longer stop\u2010signal reaction times) across age compared to non\u2010ADHD controls. When applying the novel parametric race model, this group effect was driven by higher within\u2010subject variability (sigma) and higher number of extreme responses (tau) on stop trials. The ADHD group also displayed higher within\u2010subject variability on correct responses to go stimuli. Moreover, we observed the ADHD group committing more task\u2010based failures such as responding on stop trials (trigger failures) and omissions on go trials (go failures) compared to non\u2010ADHD controls, suggesting the contribution of attentional lapses to poorer response inhibition performance. In contrast, longitudinal modelling of fixel\u2010based analysis measures revealed no significant group differences in the maturation of fronto\u2010basal\u2010ganglia fibre cross\u2010section in a subsample (74 ADHD and 73 non\u2010ADHD children). Finally, brain\u2010behavioural models revealed that age\u2010related changes in fronto\u2010basal\u2010ganglia morphology (fibre cross\u2010section) were significantly associated with reductions in the variability of the correct go\u2010trial responses (sigma.true) and skew of the stop\u2010trial distribution (tauS). However, this effect did not differ between ADHD and typically developing children. Overall, our findings support the growing consensus suggesting that attentional deficits subserve ADHD\u2010related inhibitory dysfunction. 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