When Gulsuner et al.4 mapped the 57 damaging de novo mutations they identified in persons with SZ onto transcriptome profiles of normal human brain tissues, they found that, specifically in the fetal prefrontal cortex, affected genes formed a network that functioned in neuronal migration, synaptic transmission and transcriptional regulation. These results suggest that disruptions of fetal prefrontal cortical neurogenesis are critical to the pathophysiology of SZ; consistent with this, abnormalities of cortical neuronal organization in postmortem SZ brains22 have been reported. Aberrant migration23 and distribution24 of interneurons, reduced neurite outgrowth25,26 and abnormal axon targeting27 occur in mouse models of SZ.
