Genetic analysis of interleukin-1A C(-889)T polymorphism with Alzheimer disease

Cell Mol Neurobiol. 2009 Feb;29(1):81-5. doi: 10.1007/s10571-008-9299-5. Epub 2008 Aug 15.

Abstract

Neuroinflammation has been implicated in the etiology of Alzheimer's disease (AD). Many studies have suggested that C(-889) T promoter polymorphism in one of the proinflammatory cytokine interleukin-1 (IL-1) encoding gene IL-1A may be associated with AD pathogenesis. To determine whether the polymorphism contributes to the risk for late-onset AD (LOAD) in Chinese, we carried out our investigation in 344 sporadic LOAD patients and 224 healthy controls. No statistical significant association was obtained between IL-1A C(-889) T polymorphism and LOAD and no statistical difference was found between cases and controls after stratification for apolipoprotein E allele 4 (APOE epsilon4) status. The results reveal that it is not likely that the IL-1A C(-889) T polymorphism is involved in AD pathogenesis in the Chinese population. Further studies of the associations between other IL-1A genetic polymorphisms and AD should be performed in a larger population and biologic functional analysis of IL-1A gene is required to verify the underlying roles of IL-IA in LOAD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age of Onset
  • Aged
  • Aged, 80 and over
  • Alleles
  • Alzheimer Disease / epidemiology
  • Alzheimer Disease / genetics*
  • Case-Control Studies
  • China / epidemiology
  • Female
  • Gene Frequency
  • Genetic Predisposition to Disease*
  • Heterozygote
  • Humans
  • Interleukin-1alpha / genetics*
  • Male
  • Polymorphism, Single Nucleotide / genetics*

Substances

  • Interleukin-1alpha