Cellular and molecular dysfunction in SZ has traditionally been studied by examining post-mortem patient brain tissue or through animal models. Post-mortem tissue studies are limited by degradation of key biomolecules (i.e., RNA, DNA, proteins, epigenetic marks) due to delays between death and sample processing (Ferrer et al., 2008). On the other hand, animal models carry the benefit of in vivo manipulations at different developmental stages and isogenic controls. However, animal models of SZ rely either on targeted lesions, administration of psychotropic drugs such as phencyclidine, or on manipulating a single gene associated with the disorder (Brennand and Gage, 2011; Flores et al., 2016). These approaches have limited etiological relevance, given the highly polygenic nature of SZ discussed above. By contrast, patient hiPSC-derived neurons and glia offer a unique opportunity to investigate the full genetic landscape contributing to SZ while monitoring neural development (Table 1).
