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Bipolar disorder is a serious psychiatric disorder, with a high heritability and unknown pathogenesis. Recent genome-wide association studies have identified the first loci, implicating genes such as CACNA1C and ANK3. The genes highlight several pathways, notably calcium signalling, as being of importance. Molecular studies suggest that the risk variants impact on gene regulation and expression. Preliminary studies using reprogrammed patient-derived cells report alterations in the transcriptome and in cellular adhesion and differentiation. Mouse models show that genes involved in circadian biology, acting via dopaminergic effects, reproduce aspects of the bipolar phenotype. These findings together represent significant advances in identification of the genetic and molecular basis of bipolar disorder, yet we are still far from an integrated, evidence-based understanding of its aetiopathogenesis.

Original publication

DOI

10.1016/j.conb.2015.07.002

Type

Journal article

Journal

Curr Opin Neurobiol

Publication Date

02/2016

Volume

36

Pages

1 - 6

Keywords

Animals, Ankyrins, Bipolar Disorder, Calcium Channels, L-Type, Calcium Signaling, Cell Adhesion, Cell Differentiation, Circadian Rhythm, Disease Models, Animal, Gene Expression Regulation, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Phenotype, Transcriptome