These results support the concept that many complex, neuropsychiatric disorders that are identified later in life, including BP,61, 62, 63 may result from alterations in neural differentiation that occur during development. BP neurons expressed transcripts involved in the differentiation of ventral neuronal subtypes, including FOXP2 and NKX2-1, the hallmark of the medial ganglionic eminence,51 whereas controls expressed higher levels of factors that confer (or maintain) dorsal telencephalic neuronal identity, including EMX2, PAX6, TBR2, TCF3 and ZNF536. As telencephalic neurons are involved in a number of neurodegenerative (Huntington's disease and Alzheimer's disease) and neurodevelopmental conditions (autism spectrum disorder, schizophrenia, BP and Rett syndrome), alterations in subtype specification may begin to explain the origin or susceptibility to these conditions.64 Because lithium activates WNT pathway signaling, dorsalizing early CNS progenitors,26 lithium treatment may re-direct neural stem cell fate to dorsal cortical derivatives. Many additional mechanisms may be involved, for example, FOXP2 (expressed at high levels in BP, but not control neurons) binds the DISC1 promoter,65 thereby potentially affecting cell migrations and cortical layering. There were no obvious differences in the expression of transcripts
