Association of the CR1 polymorphism with late-onset Alzheimer's disease in Chinese Han populations: a meta-analysis

Neurosci Lett. 2012 Oct 3;527(1):46-9. doi: 10.1016/j.neulet.2012.08.032. Epub 2012 Aug 27.

Abstract

It is well known that genetic variants play a critical role in the pathogenesis of Alzheimer's disease (AD). In 2009, a genome-wide association study (GWAS) demonstrated that a single nucleotide polymorphism (SNP), rs6656401, in complement receptor 1 (CR1) is significantly associated with late-onset Alzheimer's disease (LOAD) in Caucasian population. Subsequently, other researchers have attempted to validate this finding in Chinese Han populations. However, these findings in Chinese Han populations have produced both negative and positive results. To derive a more precise estimation for the relationship, we performed the present meta-analysis by analyzing three published association studies involving CR1 SNP rs6656401 through the use of the RevMan (v.5.1) program. Pooled odds ratios (ORs) were calculated for allele contrasts (A vs. G) and a dominant model [(AA+AG) vs. GG] in three studies that included 1019 cases and 1080 controls, respectively. The statistical results showed a significant difference between patients and controls for the A allele of CR1 SNP rs6656401 (P=0.005). In addition, carriers of the A allele (AA+AG) of rs6656401 had a 1.69-fold increased risk for LOAD compared with non-carriers (GG) (P=0.01). In conclusion, despite there are some limitations, this meta-analysis indicates that the A allele of the CR1 SNP rs6656401 is significantly associated with LOAD susceptibility in Chinese Han populations.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / epidemiology*
  • Alzheimer Disease / genetics*
  • China / epidemiology
  • Genetic Association Studies
  • Genetic Markers / genetics*
  • Genetic Predisposition to Disease / epidemiology*
  • Genetic Predisposition to Disease / genetics*
  • Humans
  • Polymorphism, Single Nucleotide / genetics*
  • Prevalence
  • Receptors, Complement 3b / genetics*
  • Risk Factors

Substances

  • CR1 protein, human
  • Genetic Markers
  • Receptors, Complement 3b