Correlation between MMP-3-1171 5A/6A polymorphism and the risk of Alzheimer’s disease
Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine
Background: Previous studies of matrix metalloproteinase-3 (MMP-3) -1171 5A/6A polymorphism in Alzheimer’s disease (AD) have been extensively investigated; however, the results from different studies are inconsistent. This meta-analysis was performed to clarify the link between this variant and AD. Methods: We searched PubMed, Embase, Chinese National Knowledge Infrastructure and Wanfang Database. The associations were calculated as odds ratios with the corresponding 95% confidence intervals (CIs). Results: 7 case-control studies with a total of 1457 cases and 1959 controls were included. Overall, there was no significant association between matrix metalloproteinase-3-1171 5A/6A polymorphism and AD risk in all genetic models (the allele model 5A vs. 6A: odds ratio (OR) = 1.06, 95% CI 0.82–1.36,= .65; the heterozygote model 5A/6A vs. 6A/6A: OR = 0.98, 95%CI 0.75–1.28,= .89; the homozygous model 5A/5A vs. 6A/6A: OR = 1.20, 95%CI 0.70–2.07,= .51; the dominant model 5A/6A + 5A/5A vs. 6A/6A: OR = 1.03, 95%CI 0.76–1.40,= .85; the recessive model 5A/5A vs. 5A/6A + 6A/6A: OR = 1.24, 95%CI 0.80–1.93,= .34). In subgroup analysis by ethnicity, no significant difference was detected in both Caucasians and Asians between matrix metalloproteinase-3-1171 5A/6A polymorphism and AD risk. Similar results were obtained in sensitivity analysis. Conclusion: In summary, the present meta-analysis suggests that MMP-3-1171 5A/6A polymorphism may not be associated with genetic susceptibility to AD in
Abstract
Background: Previous studies of matrix metalloproteinase-3 (MMP-3) -1171 5A/6A polymorphism in Alzheimer’s disease (AD) have been extensively investigated; however, the results from different studies are inconsistent. This meta-analysis was performed to clarify the link between this variant and AD. Methods: We searched PubMed, Embase, Chinese National Knowledge Infrastructure and Wanfang Database. The associations were calculated as odds ratios with the corresponding 95% confidence intervals (CIs). Results: 7 case-control studies with a total of 1457 cases and 1959 controls were included. Overall, there was no significant association between matrix metalloproteinase-3-1171 5A/6A polymorphism and AD risk in all genetic models (the allele model 5A vs. 6A: odds ratio (OR) = 1.06, 95% CI 0.82–1.36,= .65; the heterozygote model 5A/6A vs. 6A/6A: OR = 0.98, 95%CI 0.75–1.28,= .89; the homozygous model 5A/5A vs. 6A/6A: OR = 1.20, 95%CI 0.70–2.07,= .51; the dominant model 5A/6A + 5A/5A vs. 6A/6A: OR = 1.03, 95%CI 0.76–1.40,= .85; the recessive model 5A/5A vs. 5A/6A + 6A/6A: OR = 1.24, 95%CI 0.80–1.93,= .34). In subgroup analysis by ethnicity, no significant difference was detected in both Caucasians and Asians between matrix metalloproteinase-3-1171 5A/6A polymorphism and AD risk. Similar results were obtained in sensitivity analysis. Conclusion: In summary, the present meta-analysis suggests that MMP-3-1171 5A/6A polymorphism may not be associated with genetic susceptibility to AD in the general population. Given the limited sample size and study heterogeneity, findings warrant cautious interpretation and require verification through larger, well-designed trials.