derived cells. Neurospheres derived from the 22q11.2 deletion patients were smaller in size, had reduced expression levels of markers for cellular proliferation and survival, and an increased astrocyte to neuron ratio, consistent with observations in postmortem brains (Toyoshima et al., 2016). Integrative network analysis of hiPSC-derived neurons from eight cases with 22q11.2 microdeletion and ten healthy controls identified two sub-networks which are disrupted by 22q11.2 deletions: a cell cycle network mediated by CD45, disrupted in embryonic development, and a PRODH-mediated network, potentially contributing to disrupted brain function in adolescence when SCZ symptoms most often begin to emerge (M. Lin et al., 2016). Thus, human SCZ variants can reveal cellular developmental mechanisms linked with the disorder.
