It is well established that schizophrenia is a highly heritable, complex disease. Our understanding of its underlying pathophysiology, however, remains limited. Until recently, the systematic genome-wide search for genetic risk factors was only possible through linkage approaches, with the limitation of insufficient power to detect genes with small effects. GWA studies overcome this limitation, and the first GWA studies of schizophrenia have now been published with many more being expected to follow. In addition, large meta-analyses to increase the statistical power are currently under way. The identification of risk genes will provide a vast array of possibilities to be pursued in further research into the underlying causes of schizophrenia. One of the variants highlighted in a GWA study, the SNP in the ZNF804A gene, for example, was subsequently investigated using a functional neuroimaging approach. Esslinger et al. (2009) were able to show that risk allele carriers have reduced connectivity in the dorsolateral prefrontal cortex (DLPFC), and an increased connectivity between the DLPFC and the hippocampus formation, as well as between the amygdala and other brain regions. Disturbed interactions between different
