Other hiPSC models of SCZD have gone even further in demonstrating cellular and molecular elements of the disorder’s pathogenesis previously undetectable through post-mortem, genetic, or neuroimaging studies. Some have focused on abnormal miRNA expression profiles 129, some on cellular level deficits in adherens junction and apical polarity 43, and synaptic vesicle release deficits have also been noted 130. Furthermore, Robicsek et al. studied patient-derived hiPSCs differentiated into dopaminergic and glutamatergic neurons, in contrast to the more frequently used general forebrain differentiation program, showing perturbations in neural differentiation and mitochondrial function 131.
