remained unclear. Other data that supports such a model implicate neural stem cell or neural progenitors. For instance, mutations in the DISC1 gene have been associated with several forms of mental illness in an extended Scottish pedigree9, including BD10. DISC1 has been shown to regulate neural progenitor proliferation through inhibition of GSK3µ11, a known target of the mood stabilizer lithium signaling12–14. Furthermore antidepressant treatments have been shown to alter neural stem neurogenesis and plasticity. Thus, with what is proving to be a highly complex genetic landscape, modeling approaches investigating changes in single or small numbers of genes are incapable of capturing the full spectrum of factors that may impact pathophysiological process relevant to BD.
