Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder by Ferreira Manuel A R, O'Donovan Michael C, Meng Yan A, Jones Ian R, Ruderfer Douglas M, Jones Lisa, Fan Jinbo, Kirov George, Perlis Roy H, Green Elaine K, Smoller Jordan W, Grozeva Detelina, Stone Jennifer, Nikolov Ivan, Chambert Kimberly, Hamshere Marian L, Nimgaonkar Vishwajit L, Moskvina Valentina, Thase Michael E, Caesar Sian, Sachs Gary S, Franklin Jennifer, Gordon-Smith Katherine, Ardlie Kristin G, Gabriel Stacey B, Fraser Christine, Blumenstiel Brendan, Defelice Matthew, Breen Gerome, Gill Michael, Morris Derek W, Elkin Amanda, Muir Walter J, McGhee Kevin A, Williamson Richard, MacIntyre Donald J, MacLean Alan W, St Clair David, Robinson Michelle, Van Beck Margaret, Pereira Ana C P, Kandaswamy Radhika, McQuillin Andrew, Collier David A, Bass Nicholas J, Young Allan H, Lawrence Jacob, Ferrier I Nicol, Anjorin Adebayo, Farmer Anne, Curtis David, Scolnick Edward M, McGuffin Peter, Daly Mark J, Corvin Aiden P, Holmans Peter A, Blackwood Douglas H, Gurling Hugh M, Owen Michael J, Purcell Shaun M, Sklar Pamela, Craddock Nick, Wellcome Trust Case Control Consortium in Nature genetics (2008).

[PMID: 18711365] PubMed


To identify susceptibility loci for bipolar disorder, we tested 1.8 million variants in 4,387 cases and 6,209 controls and identified a region of strong association (rs10994336, P = 9.1 x 10(-9)) in ANK3 (ankyrin G). We also found further support for the previously reported CACNA1C (alpha 1C subunit of the L-type voltage-gated calcium channel; combined P = 7.0 x 10(-8), rs1006737). Our results suggest that ion channelopathies may be involved in the pathogenesis of bipolar disorder.

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