Complement receptor 1 genetic polymorphism contributes to sporadic Alzheimer's disease susceptibility in Caucasians:
Hai Yuan1, Lingling Du1, Pingping Ge1
1Department of Rehabilitation Medicine, The Second People's Hospital of Hefei City, Hefei, China.
Insights
Genetic variations in Complement Receptor 1 (CR1) are linked to an increased risk of developing sporadic Alzheimer's disease (SAD) in Caucasian populations. This meta-analysis confirms the association between CR1 polymorphisms and SAD susceptibility.
Area of Science:
- Neuroscience
- Genetics
- Immunology
Background:
- Complement receptor 1 (CR1) is implicated in sporadic Alzheimer's disease (SAD) pathogenesis in Caucasians.
- Previous studies on the association between CR1 genetic polymorphisms (rs6656401A/G and rs3818361T/C) and SAD risk have yielded controversial results.
Purpose of the Study:
- To conduct a comprehensive meta-analysis to clarify the association between CR1 genetic polymorphisms (rs6656401A/G and rs3818361T/C) and the risk of SAD in Caucasian individuals.
Main Methods:
- A meta-analysis was performed, aggregating data from 18 case-control studies.
- Statistical analyses included dominant, recessive, homozygote, and heterozygote comparisons for CR1 rs6656401A/G and rs3818361T/C polymorphisms.
Main Results:
- CR1 rs6656401A/G polymorphism showed a statistically significant association with SAD risk across multiple genetic models (dominant, recessive, homozygote, heterozygote).
- CR1 rs3818361T/C polymorphism also demonstrated a significant association with SAD risk in dominant, recessive, homozygote, and heterozygote comparisons.
- Carriers of the rs6656401 A allele or the rs3818361 T allele in CR1 may represent an increased risk factor for SAD in Caucasians.
Conclusions:
- The meta-analysis provides robust evidence that CR1 rs6656401A/G and rs3818361T/C polymorphisms are associated with an increased risk of sporadic Alzheimer's disease in Caucasian populations.
- These findings highlight the role of CR1 genetic variations in SAD development and may inform future risk assessment strategies.
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.
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