Though the characteristic symptoms of schizophrenia (SZ) generally appear late in adolescence, it is thought to be a neurodevelopmental condition1 that is often predated by a prodromal period that can appear in childhood.2 Although postmortem studies have identified defects in neurons, such as reduced neuronal size and spine density in the prefrontal cortex and hippocampus,3 these findings represent disease end points and reveal little about disease predisposition or initiation. Because damaging de novo mutations in persons with SZ converge in a network of genes co-expressed in the prefrontal cortex during fetal development,4 one prevailing hypothesis is that disruptions in fetal prefrontal cortical development underlie SZ.
