Neuroimaging findings from the COS cohort are consistent with the AOS literature showing increased lateral ventricular volume, decreased total and regional cortical GM volumes, decreased hippocampal and amygdala volumes, and increased basal ganglia volumes that progressed during adolescence (see Gogtay and Rapoport, 2008, for review). Most strikingly revealed by longitudinal data is progressive cortical GM loss during adolescence (Thompson et al., 2001) and delayed white matter development (Gogtay et al., 2008). The cortical GM reduction becomes more circumscribed with age (as the healthy group trajectory of cortical thinning “catches up” with the accelerated pattern of cortical GM loss seen in COS). The cortical GM loss in schizophrenia has been shown to be due to the loss of “neuropil,” which consists of glia, synaptic and dendritic arbors, and vasculature (Selemon and Goldman-Rakic, 1999). Postmortem studies show no widespread neuronal loss in schizophrenia or a glial response to a potential neuronal injury. Based on these and other converging data, developmental models of abnormal synaptic function or structure have predominated (Weinberger et al., 1992).
