that these normative gene–brain relationships would be disrupted in patients with COS. We also studied the unaffected SIBs of COS probands as a way to test if any observed alterations of gene–brain relationships in COS patients reflected the consequences of active illness (e.g. treatment with DA modifying drugs) rather than familial/trait markers of risk for schizophrenia. Longitudinal assessment of the relationships between genetic and neuroanatomical variation is especially important in this context because abnormal patterns of anatomical change over time are a well-established correlate of risk for schizophrenia (Gogtay, 2008). Also, more generally, genetic influences in brain anatomy are not developmentally stable (Lenroot et al., 2009), and differ for longitudinal as opposed to static measures of brain anatomy (Brans et al., 2010).
