Complement receptor 1 genetic polymorphism contributes to sporadic Alzheimer’s disease susceptibility in Caucasians: A meta-analysis

Abstract

Complement receptor 1 (CR1) plays an important role in the development of sporadic Alzheimer’s disease (SAD) in Caucasians. However, the influence of CR1 (rs6656401A/G and rs3818361T/C) genetic polymorphisms on the risk of SAD remains controversial. A meta-analysis of 18 case–control studies was performed to derive a more precise association of CR1 (rs6656401A/G or rs3818361T/C) genetic polymorphism with the risk of SAD in Caucasians. A statistical difference was found in the dominant model (odds ratio (OR): 1.23, 95% confidence interval (CI): 1.16–1.30, P=0.00), recessive model (OR: 1.28, 95% CI: 1.05–1.56, P=0.02), homozygote comparison (OR: 1.36, 95% CI: 1.12–1.66, P=0.002) or heterozygote comparison (AG versus GG) (OR: 1.21, 95% CI: 1.15–1.29, P=0.00) of CR1 rs6656401A/G. For CR1 rs3818361T/C, a statistical difference was observed in the dominant model (OR: 1.21, 95% CI: 1.13–1.31, P=0.00), recessive model (OR: 1.28, 95% CI: 1.07–1.53, P=0.006), homozygote comparison (OR: 1.35, 95% CI: 1.13–1.62, P=0.001) or heterozygote comparison (TC versus CC) (OR: 1.20, 95% CI: 1.11–1.29, P=0.00). In summary, despite some limitations, the present meta-analysis indicated that rs6656401A/G or rs3818361T/C polymorphism was related to SAD risk. Moreover, a carrier of rs6656401A/G or T carrier of rs3818361T/C in CR1 genetic polymorphism might be an increased factor for SAD in Caucasians.