These important limitations notwithstanding, the evidence is growing of genetic vulnerability maps of the brain and the way in which they are modulated by risk genes in psychiatry. To date, a consistent observation in unaffected relatives of patients with schizophrenia is abnormal PFC and inferior parietal lobule activation, across different executive cognitive paradigms, and an abnormal lateralization of prefrontal-temporal areas during verbal fluency. These neuroimaging phenotypes have been most frequently studied in relation to schizophrenia-risk genes. Interestingly, there appear to be specific effects of genes on some neuroimaging intermediate phenotypes but not on others, suggesting discrete biological mechanisms of risk in some but not all brain areas/circuits and their related cognitive functions. On the other hand, there are still important gaps between the data on “imaging genetics” and the data on intermediate phenotypes. Many schizophrenia risk genes have been shown to modulate circuits that have not yet been demonstrated to be intermediate phenotypes (e.g. genes modulating prefrontal cortex coupling during working memory tasks or genes modulating hippocampus activity during episodic memory), and not all reported neuroimaging intermediate phenotypes have been
