tissue (Chen et al., 2004). Increased DA catabolism imparted by the Val allele is thought to result in reduced synaptic DA availability, with consequences for PFC function that vary according to background dopaminergic tone (Tunbridge et al., 2006). Thus, comparing the relationship between Val158Met genotype and developmental changes in cortical anatomy between people with COS and HCs would provide information about the integrity of dopaminergic influences upon cortical maturation in schizophrenia. Preliminary evidence that these influences are disrupted in people with schizophrenia comes from cross-sectional neuroimaging reports that the structural (Ohnishi et al., 2006), and functional (Prata et al., 2009) cortical correlates of Val158Met genotype differ between people with schizophrenia and HCs in cingulate, dlPFC and lateral temporal regions. Our current study represents the first to (i) relate to Val158Met genotype to longitudinal measures of anatomical change in people with schizophrenia, and (ii) also do so in the healthy siblings of probands as a way of assessing gene–brain relationships in the absence of disease-related confounds.
