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Original Research

Significant association of BDNF rs6265 G>A polymorphism with susceptibility to epilepsy: a meta-analysis

, , , , , , & show all
Pages 1035-1046 | Published online: 16 Apr 2018
 

Abstract

Introduction

Previously published articles have suggested that BDNF rs6265 G>A polymorphism is a potential risk factor for epilepsy. However, the results were not consistent.

Methods

We conducted a meta-analysis to explore the association between BDNF rs6265 G>A polymorphism and epilepsy risk. Four online databases were searched, and related studies were reviewed from their inception up to June 20, 2017. ORs and corresponding 95% CIs were used to calculate the associations of each genetic model. Overall, 10 case–control publications involving 9,512 subjects were included in this meta-analysis.

Results

Significant associations were found between BDNF rs6265 G>A polymorphism and epilepsy (A vs G: OR=0.88, 95% CI=0.83–0.94, P<0.01, I2=0%; GA vs GG: OR=0.88, 95% CI=0.79–0.97, P=0.01, I2=0%; AA vs GG: OR=0.79, 95% CI=0.70–0.90, P<0.01, I2=0%; GA+AA vs GG: OR=0.85, 95% CI=0.77–0.94, P<0.01, I2=0%; AA vs GG+GA: OR=0.85, 95% CI=0.76–0.95, P=0.01, I2=0%). Subgroup analysis also showed similar results in an Asian population.

Conclusion

Our meta-analysis indicated that BDNF rs6265 G>A polymorphism might be involved in epilepsy susceptibility, especially in the Asian population.

Supplementary materials

Figure S1 OR and 95% CIs of the associations between BDNF rs6265 G>A polymorphism and epilepsy susceptibility (A for A vs G model; B for GA vs GG model; C for AA vs GG model; and D for AA vs GG+GA model).

Figure S1 OR and 95% CIs of the associations between BDNF rs6265 G>A polymorphism and epilepsy susceptibility (A for A vs G model; B for GA vs GG model; C for AA vs GG model; and D for AA vs GG+GA model).

Figure S2 Sensitivity analysis through deleting each study to reflect the influence of the individual dataset to the pooled ORs in BDNF rs6265 G>A polymorphism and epilepsy susceptibility (A for A vs G model; B for GA vs GG model; C for AA vs GG model; and D for AA vs GG+GA model).

Figure S2 Sensitivity analysis through deleting each study to reflect the influence of the individual dataset to the pooled ORs in BDNF rs6265 G>A polymorphism and epilepsy susceptibility (A for A vs G model; B for GA vs GG model; C for AA vs GG model; and D for AA vs GG+GA model).
Figure S2 Sensitivity analysis through deleting each study to reflect the influence of the individual dataset to the pooled ORs in BDNF rs6265 G>A polymorphism and epilepsy susceptibility (A for A vs G model; B for GA vs GG model; C for AA vs GG model; and D for AA vs GG+GA model).

Figure S3 Cumulative meta-analyses according to publication year in BDNF rs6265 G>A polymorphism and epilepsy susceptibility (A for A vs G model; B for GA vs GG model; C for AA vs GG model; and D for AA vs GG+GA model).

Figure S3 Cumulative meta-analyses according to publication year in BDNF rs6265 G>A polymorphism and epilepsy susceptibility (A for A vs G model; B for GA vs GG model; C for AA vs GG model; and D for AA vs GG+GA model).

Figure S4 Funnel plot analysis to detect publication bias in BDNF rs6265 G>A polymorphism and epilepsy susceptibility (A for A vs G model; B for GA vs GG model; C for AA vs GG model; and D for AA vs GG+GA model).

Figure S4 Funnel plot analysis to detect publication bias in BDNF rs6265 G>A polymorphism and epilepsy susceptibility (A for A vs G model; B for GA vs GG model; C for AA vs GG model; and D for AA vs GG+GA model).

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Acknowledgments

This study was supported by the Foundations of the Science and Technology Department of Hubei Province (no 2016CFB567) and Taihe Hospital (2016BSQD02). These organizations had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Disclosure

The authors report no conflicts of interest in this work.