Thus, it is valuable to search for SZ-specific changes in early neural development of individuals containing the 22q11.2 deletion. However, research on the biological basis of SZ and other neuropsychiatric disorders has been hampered by the inaccessibility of developing human brains. This problem has been partially circumvented by iPSC technology [22], which allows investigators to grow patient-specific neurons or neuroaggregates [23, 24] for modeling in vitro the cellular developmental abnormalities associated with psychiatric disorders. In the past few years, investigators have successfully applied this strategy and established iPSC lines in a variety of brain disorders including Rett Syndrome, Parkinson Disease, Amyotrophic Lateral Sclerosis, Familial Dysautonomia, and most recently, SZ [25–30].
