One of the mainstream theories behind the pathogenesis of SCZ is dopamine dysregulation. Studies supporting this theory show aberrant dopamine transmission within multiple brain regions,69 including the amygdala,70 prefrontal cortex71, 72 and hippocampus.73 Our group has established an efficient differentiation protocol for generating midbrain dopaminergic neurons, which showed long-term survival when engrafted in mouse, rat and monkey models.74 Numerous groups have used and adapted this protocol for the generation of dopaminergic neurons from patients with SCZ.75, 76 Dopaminergic neurons differentiated from iPSCs derived from patients with SCZ had a reduced neurite count and dopamine release and showed delayed maturation.76 Interestingly, these defective neurons exhibited perturbations in mitochondrial network structure and connectivity. This suggests a potential mitochondrial defect having a key role in the pathogenesis of SCZ, much like that reported in BPD.63 Reports indicating that iPSCs from some patients with SCZ show poor differentiation into dopaminergic neurons,75 suggesting a need to improve current protocols before those neurons can serve as a robust platform to study the factors contributing to the dysregulation of dopamine in SCZ. Such further improvements may also
