There is a strong neurodevelopmental component to SZ risk (Weinberger, 1995). Most cases of SZ are diagnosed in adolescence or young adulthood (Lewis and Lieberman, 2000), although there are rare cases of childhood onset (Asarnow, 1994). During these stages of development, extensive synaptic pruning and overall loss of gray matter occurs (Huttenlocher and Dabholkar, 1997). Neuroimaging studies have shown a loss of frontal and hippocampal volume in SZ patients; post-mortem tissue analyses have further identified decreased spine density and synaptic connectivity (Glantz and Lewis, 2000; McGlashan and Hoffman, 2000; Faludi and Mirnics, 2011). Microglia and oligodendrocytes have also been implicated in SZ pathology, due to their roles in synaptic pruning (Paolicelli et al., 2011) and cell-to-cell communication (Tkachev et al., 2003), respectively.
