These results showed an abnormal dispersion of the proliferating stem-like cells outside the VZ into the IZ and CZ, and a curtailed neuronal cortical development in the CZ of the schizophrenia cerebral organoids accompanied by turning off the expression of nFGFR1. The arrest of cortical development was reproduced in control cerebral organoids derived from hESCs, by blocking and depleting FGFR1 with its specific antagonist, PD173074. This study suggests that a reconstitution of nFGFR1 in developing cortical neurons can modify the developmental malformations.
