Research press release


Nature Genetics

Ion channels implicated in bipolar disorder

2つの遺伝子の多型が双極性障害の高い発症リスクと関連していることを報告する研究論文が、Nature Genetics(電子版)に掲載される。双極性障害は、一般的な気分障害で、かつては躁うつ病と呼ばれ、躁状態とうつ状態が交互に現れるという特徴がある。

既に公表されている全ゲノム関連解析で、双極性障害の遺伝的危険因子を示唆する証拠が得られているが、すべての解析結果を通してみると、一致点はほとんどない。今回、マサチューセッツ総合病院(米国ボストン)のP SklarとS Purcell、そしてカーディフ大学(英国)のN Craddockがリーダーを務めた共同研究では、公表されている結果を再度解析し、それに加えて、別の双極性障害の患者グループについてゲノム関連解析を行った。


Variants in two genes are associated with increased risk of bipolar disorder, according to a study published online this week in Nature Genetics. Bipolar disorder is a common mood disorder formerly known as manic depression, and is characterized by alternating episodes of mania and depression.

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.

doi: 10.1038/ng.209


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