Converging evidence from new epidemiologic, genetic, epigenetic, neuroimaging, and experimental model findings are further refining a long-standing concept, regarding the underlying neurobiology of attention-deficit/hyperactivity disorder (ADHD): that ADHD onset and its persistence into adulthood are the result of dysregulated myelination and associated alterations in neuronal plasticity - linked to disrupted brain maturation and the persistence of cognitive and emotional impairments across the life span. If supported by further work, this concept represents a pathophysiologic mechanism amenable to therapeutic intervention.