AKT1 and genetic vulnerability to bipolar disorder
| Autor: | Granville J. Matheson, Lina Martinsson, Catharina Lavebratt, Inger Römer Ek, Martin Schalling, Lena Backlund, Vincent Millischer |
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| Rok vydání: | 2019 |
| Předmět: |
Adult
Male Psychosis Bipolar Disorder AKT1 Single-nucleotide polymorphism Genome-wide association study Biology Polymorphism Single Nucleotide Cohort Studies 03 medical and health sciences 0302 clinical medicine medicine Humans Genetic Predisposition to Disease Bipolar disorder Gene Biological Psychiatry Genetic association Genetics Sweden Haplotype Middle Aged medicine.disease 030227 psychiatry Psychiatry and Mental health embryonic structures Female Proto-Oncogene Proteins c-akt 030217 neurology & neurosurgery Genome-Wide Association Study |
| Zdroj: | Psychiatry research. 284 |
| ISSN: | 1872-7123 |
| Popis: | AKT1 encodes a serine/threonine kinase that has as one of its best-known substrates glycogen synthase kinase-3 (GSK3), a primary target for lithium. AKT1 has been previously been implicated as a vulnerability gene for bipolar disorder (BD). We aimed to associate genetic variants in the AKT1 gene with subgroups of BD. BD patients from a Swedish cohort (N = 831) were phenotyped in regards to their psychotic episodes according to mood-congruence in depression and manias, and compared to controls (N = 1,496). All participants were genotyped for SNPs in AKT1 previously implicated to have a role: rs3730358, rs1130214 and rs3803300. None of the effects reported in earlier studies were statistically significant, including the association between rs3803300 and BD without any psychotic symptoms, rs3803300 and mood-congruent psychosis, rs3803300 and the combined groups, as well as the association between the haplotypes formed by rs3730358 and rs1130214 and risk for BD. In a Bayesian analysis, all Bayes’ Factors using default priors supported the null hypothesis in the replication set by a factor of between 5 and 1300 times. Analysis of genome wide association data did not reveal any association between BD and the AKT1 region. We conclude AKT1 is less likely to be a vulnerability gene in BD. |
| Databáze: | OpenAIRE |
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