The involvement of GSK3beta in bipolar disorder: integrating evidence from multiple types of genetic studies.
|Title||The involvement of GSK3beta in bipolar disorder: integrating evidence from multiple types of genetic studies.|
|Publication Type||Journal Article|
|Year of Publication||2010|
|Authors||Luykx, JJ, Boks MPM, Terwindt APR, Bakker S, Kahn RS, Ophoff RA|
|Journal||European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology|
|Date Published||2010 Jun|
|Keywords||Animals, Bipolar disorder, Data Collection, Disease Models, Animal, Epigenesis, Genetic, Gene Expression Regulation, Enzymologic, Genetic Linkage, Genetic Predisposition to Disease, Genome-Wide Association Study, Glycogen Synthase Kinase 3, Humans, Mice, Pharmacogenetics|
We aimed to get a comprehensive insight into the genetic evidence supporting the role of GSK3beta in bipolar disorder (BD). Using broad searches in NCBI's PubMed and the Genetic Association Database we looked for association, whole-genome linkage, genome-wide association, gene expression, pharmocogenomic, epigenetic, cytogenetic, and mouse model studies performed for BD until July 2009. Per gene, we rated the degree of converging evidence across these types of genetic studies. The genes most consistently associated with BD in the genetic studies we reviewed were GSK3beta , GRK3, 5-HTTLPR, GRIN3, COMT, and GLUR3. GSK3beta stood out as it was implicated in at least five types of genetic studies. Although our results are limited by design differences of included studies and possibly by publication bias, GSK3beta is a plausible candidate gene for BD from a pharmacological and a genetic perspective. Future studies investigating the effects of GSK3beta manipulation in BD seem warranted.
|Alternate Journal||Eur Neuropsychopharmacol|