Ion Channels Implicated In Bipolar Disorder

Previously published genome-wide association studies have generated suggestive evidence for genetic risk factors, although with little agreement from study to study. Pamela Sklar, Nick Craddock and Shaun Purcell led a collaborative effort to re-analyze the published results in combination with a genome scan of an additional group of individuals with the disease.

The strongest evidence for genetic risk factors was for variants in ANK3 and CACNA1C. The gene ANK3 encodes a protein called ankyrin G, which has been reported to regulate the assembly of sodium channels. The gene CACNA1C, encoding a calcium channel subunit, provides support for an association that had previously been suggested. Some of the authors had also previously shown that both these genes are down-regulated in the mouse brain in response to lithium, which is one of the most effective therapies for bipolar disorder. The data raise the possibility that bipolar disorder is, in part, a result of altered ion channel function.

Author contacts:

Pamela Sklar (Massachusetts General Hospital, Boston, MA, USA)
E-mail: sklar@chgr.mgh.harvard.edu

Nick Craddock (Cardiff University, UK)
E-mail: craddockn@cardiff.ac.uk

Shaun Purcell (Massachusetts General Hospital, Boston, MA, USA)
E-mail: shaun@pngu.mgh.harvard.edu

Abstract available online.

(C) Nature Genetics press release.

Message posted by: Trevor M. D'Souza