Figure 1.

Pathophysiological alterations observed in iPSC models of schizophrenia and bipolar disorder. The development of 2- and 3-dimensional iPSC models has allowed the investigation of several, often interconnected, pathophysiological mechanisms that appear to contribute to the clinical presentation of schizophrenia and bipolar disorder. Research using iPSCs has reinforced the idea that these disorders share different neurobiological mechanisms, as shown by the detection of disturbances in neurodevelopmental processes (proliferation, segmentation, and differentiation), neuromorphological alterations (axon development, myelination, and dendrite branching), glutamatergic–GABAergic transmission imbalance (also linked to dysfunctions in dopaminergic pathways), and defects in ion channels and mitochondria, in both disorders. DA = dopamine, iPSC = induced plurpipotent stem cell, GABA = γ-aminobutyric acid, NMDA = N-methyl-D-aspartate.