human oligodendroglia was similarly lower in the callosal white matter of SCZ hGPC chimeras, than in control hGPC chimeras (8,778±892.2/mm3, n=25; vs. 17,754±2,023/mm3, n=17, respectively; p=0.0006, Mann-Whitney) (Figure 2J). These data indicate that SCZ GPCs are deficient not only in their colonization of the forebrain white matter, but also in their oligodendrocytic differentiation, with a resultant suppression of central myelinogenesis. Together, these findings suggest that SCZ hGPCs migrate aberrantly, traversing rather than homing to developing white matter, thus yielding relatively poor white matter engraftment, deficient myelin formation, and premature cortical entry relative to normal GPCs.
