Schizophrenia is a highly heritable (Cardno et al., 1999) neurodevelopmental disorder that is strongly associated with dopaminergic dysregulation (Howes and Kapur, 2009; Simpson et al., n.d.), and maturational (Brans et al., 2008; Thompson et al., 2001; Vidal et al., 2006) and functional (Minzenberg et al., 2009) abnormalities in higher-order fronto-temporal and parietal “associative” cortices sub-serving executive function and language. Similar, but less pronounced dopaminergic (Hirvonen et al., 2006) and maturational (Gogtay et al., 2007) alterations also exist in non-psychotic individuals considered to be at elevated risk for schizophrenia based on a family history of schizophrenia, or a personal history of prodromal symptoms. Twin and family studies suggest that such alterations of dopamine (DA) signaling (Hirvonen et al., 2006) and structural cortical maturation (Brans et al., 2008; McDonald et al., 2006) directly index genetic liability for schizophrenia.
