into the molecular changes of BPD by reducing both genetic and non- genetic variability, but moreover, might leverage the existing genetic data from this pedigree. The iPSC lines from 4 affected and 4 unaffected relatives were differentiated into neuroprogenitors (NPs) and neurons in vitro. Using microarray analysis, we confirmed stages of differentiation of the iPSCs to neurons by characteristic gene expression patterns, and observed a subset of differentially expressed genes (DEGs) between BPD subjects and their healthy siblings only in L neurons. Hierarchical clustering and pathway analyses revealed differences in genes involved in RNA biosynthesis, protein trafficking and receptor signaling pathways.
