The precise relationship between the etiology and cellular pathophysiology of bipolar disorder (BD) remains poorly understood1–3. In light of its high heritability4,5, genome-wide association studies (GWAS) have been used to identify genes and pathways associated with BD risk. Several GWAS and their meta-analyses have reported several genomic loci that meet the criteria of genome-wide significance5–7. However, despite these genetic efforts the biological basis of BD remains elusive and the path toward highly effective, disease-modifying, targeted therapeutics is uncertain. Measurable brain pathology has had limited success as well; consistent neuroanatomical deficits have been difficult to identify. Some of the most consistent imaging results have implicated grey matter changes in both emotion and reward processing circuits8. Anatomical deficits such as these brain volume changes have prompted some researchers to label BD a “neurodevelopmental” disorder, but the basis for such neurodevelopmental deficits has 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
