ABSTRACT
Scientific background Although the aetiology of ADHD is incompletely understood, increasing evidence strongly supports a biological basis.
■ Heritability of ADHD estimated as greater than 0.7. ■ Molecular genetics:
– Replicated evidence implicating dopamine (DA) genes (D4, D5, the DA transporter)
– Preliminary evidence implicating D1 and 5-HT1B, DA-β-hydroxylase and synaptosomal-associated protein 25 (SNAP-25, involved in the regulation of neurotransmitter release)
– Polygenic with small contribution from each gene (odds ratios [ORs], 1.2-1.9)
■ Evidence for contribution to risk of developing ADHD from – Antenatal and perinatal factors (e.g. alcohol, nicotine, low birth-
weight, obstetric complications, possibly intrauterine valproate exposure)
– Environmental pollutants such as lead, polychlorinated biphenyls (PCBs) and mercury
■ Structural/functional abnormalities have been shown in many brain regions including frontal, temporal and parietal cortical regions, basal ganglia, callosal areas and cerebellum.
