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.

Bioscience Reports
|May 21, 2020
PubMed

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.

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