in Disrupted in Schizophrenia 1 (DISC1), which encodes a protein involved in neurite outgrowth and cortical development (Wen et al., 2014; Ye et al., 2017), have been generated. Neurons derived from iPS cells harboring DISC1 mutations had synaptic defects, and genes that correlate to synaptic transmission and development were also improperly regulated (Soliman, Aboharb, Zeltner, & Studer, 2017). The power of patient derived iPS cells in modeling SCZ is quite clear from this study for two main reasons: 1) 90 of the identified genes that were dysregulated in neurons carrying the DISC1 mutation had been previously linked to mental disorders such as SCZ. 2) Gene editing was used to correct the DISC1 mutation upon which disease phenotypes were reversed, indicating that the effects observed on cellular phenotype, as well as gene expression, was a direct consequence of the patient derived DISC1 mutation. This illustrates how patient derived iPS cells can be used to understand the precise cellular mechanisms caused by a mutation linked to a certain disease.
