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Association of CD14-260 (-159) C/T and Alzheimer’s disease: systematic review and trial sequential analyses

Current studies have evaluated the association between CD14-260 (also known as -159) C/T polymorphism and Alzheimer’s disease (AD) susceptibility. However, the association remains inconclusive. The aim of this study was to draw an accurate conclusion of the association. The literature search was con...

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Bibliographic Details
Published in:Journal of Neural Transmission 2018-09, Vol.125 (9), p.1313-1318
Main Authors: Wang, Yan, Wu, Xiaoling, Deng, Xun, Ma, Yanjiao, Huang, Siyi, Wang, Yong
Format: Article
Language:English
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Summary:Current studies have evaluated the association between CD14-260 (also known as -159) C/T polymorphism and Alzheimer’s disease (AD) susceptibility. However, the association remains inconclusive. The aim of this study was to draw an accurate conclusion of the association. The literature search was conducted using PubMed, Embase, Chinese National Knowledge Infrastructure, China Biological Medicine Database, and Wanfang Databases for related articles. Four case–control studies with a total of 868 cases and 766 controls were eligible to be included in this meta-analysis. The association was evaluated by calculating the odds ratios (ORs) with the corresponding 95% confidence intervals (CIs). Overall, there was no significant association between CD14-260C/T polymorphism and AD risk in all genetic models (the allele model T vs. C: OR = 1.06, 95% CI 0.92–1.21, p  = 0.44; the homozygous model TT vs. CC: OR = 1.09, 95% CI 0.83–1.44, p  = 0.53; the heterozygote model CT vs. CC: OR = 0.95, 95% CI 0.75–1.22, p  = 0.71; the dominant model TT + CT vs. CC: OR = 1.05, 95% CI 0.84–1.32, p  = 0.66; the recessive model TT vs. CT + CC: OR = 1.14, 95% CI 0.92–1.43, p  = 0.24). The sample size of 5064 was calculated by applying trial sequential analysis. Cumulative z curve does not cross trial sequential monitoring boundary. In conclusion, the present meta-analysis suggests that the CD14-260C/T polymorphism may not be associated with genetic susceptibility of AD, but the association remains indeterminate due to the insufficient evidence.
ISSN:0300-9564
1435-1463
DOI:10.1007/s00702-018-1896-y