TPH2 gene polymorphisms and bipolar disorder: A meta-analysis
Autor: | Jingxuan Zhang, Mingrui Jia, Dongdong Qiao, Jeremy Sokolove, Huimin Qiu, Zhenglun Pan, Jin Gao |
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Rok vydání: | 2014 |
Předmět: |
Linkage disequilibrium
Bipolar Disorder Single-nucleotide polymorphism Biology Tryptophan Hydroxylase Polymorphism Single Nucleotide 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Gene Frequency medicine Humans Genetic Predisposition to Disease Bipolar disorder Allele frequency Genetics (clinical) Genetic Association Studies Genetic association Genetics TPH2 Random effects model medicine.disease 030227 psychiatry Psychiatry and Mental health Meta-analysis 030217 neurology & neurosurgery |
Zdroj: | American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics. (2) |
ISSN: | 1552-485X |
Popis: | Background: Disturbance of the serotonergic system contributes to the etiology of bipolar disorder (BD). Tryptophan hydroxylase-2 (TPH2) is an important rate-limiting enzyme in the synthetic pathway for brain serotonin and has been suggested to play a role in BD. Materials and methods: We performed a systematic review and meta-analysis of all studies to date investigating the association studies between TPH2 and BD published before Aug 2014. All studies were abstracted from PubMed, Embase, HuGNet, and China National Knowledge Infrastructure (CNKI). Manuscripts and the supplementary documents of published genome-wide association studies in the field were also included. Effect sizes of independent loci that have been studied in more than three articles were synthesized using fixed and random effects models. Results: Eight eligible studies addressed association between 63 TPH2 gene single nucleotide polymorphisms (SNPs) with BD, after linkage disequilibrium analysis, 12 independent SNPs were identified. Finally, three SNPs (rs4760820, rs11178998, and rs7954758) were found associated with BD using fixed effects models, and rs4760820 and rs11178998 were still associated with BD even with the more conservative random effects models. Conclusions: rs4760820 and rs11178998 were identified to have strong genetic association with BD in present study though confirmation will require larger sample sizes and in additional populations. © 2015 Wiley Periodicals, Inc. |
Databáze: | OpenAIRE |
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