SynthesisMolecular biology reports2014
Meta-analysis demonstrates lack of association of the GSK3B -50C/T polymorphism with risk of bipolar disorder.
Synthesis in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 2 syntheses or guidelines pooled it, 8 citations in OpenAlex.
- Pooled it
- The genetics of early-onset bipolar disorder: A systematic review.Journal of affective disorders · 2015Pooled it
- Genetic Variants Involved in Bipolar Disorder, a Rough Road Ahead.Clinical practice and epidemiology in mental health : CP & EMH · 2018Article
- Role of GSK3β in breast cancer susceptibility.Cancer biomarkers : section A of Disease markers · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Published data on the association between GSK3B -50C/T (rs334558) and bipolar disorder (BD) are inconclusive. We performed this meta-analysis to evaluate the relationship of this single-nucleotide polymorphism with the susceptibility, and with the age at onset of BD. A literature search was conducted though PubMed, EMBASE, Web of Science and China National Knowledge Infrastructure databases to identify relevant studies up to February 14, 2014. We identified a total of 6 publications including 1,251 cases and 1,804 controls to investigate the effect of GSK3B -50C/T on BD risk, and found no significant association in any genetic models (C vs. T: OR = 1.03, 95 % CI: 0.92-1.15; CC vs. TT+TC: OR = 1.04, 95 % CI: 0.84-1.28; TC+CC vs. TT: OR = 1.16, 95 % CI: 0.97-1.39; and CC vs. TC vs. TT: OR = 1.08, 95 % CI: 0.96-1.22). Subgroup analysis by ethnicity did not change the results. The association between GSK3B -50C/T and age at onset of BD was explored by 6 identified studies with a total of 659 BD type I patients. Similarly, we did not observe significant results in any genetic models (TC+CC vs. TT: SMD = 0.20, 95 % CI: -0.07 to 0.47; CC vs. TT+TC: SMD = 0.11, 95 % CI: -0.10 to 0.32; CC vs. TT: SMD = 0.32, 95 % CI: -0.13 to 0.77). The power analysis and tests for publication bias ensured the reliability of our results. In summary, this meta-analysis suggests that the functional polymorphism -50C/T within the GSK3B gene promoter is unlikely to relate with BD risk. However, more larger and well-designed studies are still needed to yield a conclusive result on the topic.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.