Published in:
01-12-2018 | Neurology and Preclinical Neurological Studies - Review Article
Correlation between MCP-1-2518A/G polymorphism and the risk of Alzheimer’s disease
Authors:
Yan Wang, Siyi Huang, Xiaoling Wu, Yong Wang, Deqi Jiang
Published in:
Journal of Neural Transmission
|
Issue 12/2018
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Abstract
The -2518A/G polymorphism in monocyte chemotactic protein-1 (MCP-1) has been extensively investigated for association with Alzheimer’s disease (AD); however, the results from different studies are inconsistent. The aim of this study was to draw an accurate conclusion of the association. All eligible case–control studies were searched in PubMed, Embase, Chinese National Knowledge Infrastructure, China Biological Medicine Databases, and Wanfang Databases. Eight case–control studies with a total of 2370 cases and 2413 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 MCP-1-2518A/G polymorphism and AD risk in all genetic models (the allele model G vs. A: OR = 1.15, 95% CI 0.92–1.45, p = 0.22; the co-dominant model GG vs. AA: OR = 1.38, 95% CI 0.80–2.36, p = 0.25; the dominant model AG + GG vs. AA: OR = 1.14, 95% CI 0.89–1.46, p = 0.31; the recessive model GG vs. AG + AA: OR = 1.35, 95% CI 0.87–2.09, p = 0.18). In subgroup analysis by ethnicity, a significant difference was not detected in both Caucasians and Asians. In allele model (G vs. A), the required sample size of 31858 was calculated by applying trial sequential analysis. Cumulative z curve is always below the trial sequential monitoring boundary and is nominally statistically significant (Z = 1.96). A consistent result was obtained in other genetic models. In summary, the present meta-analysis suggests that MCP-1-2518A/G polymorphism may not be associated with genetic susceptibility of AD in general population, but the association remains indeterminate due to the insufficient evidence.