Genomics Inform.  2004 Jun;2(2):81-85.

No Evidence of Association of Interleukin 1A(-889) Genetic Polymorphism with Alzheimer's Disease in Koreans

Affiliations
  • 1Department of Psychiatry, Pundang Jesaeng Hospital,Daejin Medical Center, Seongnam, Kyunggi, Korea.
  • 2Department of Biochemistry and Molecular Biology, College of Medicine, Seoul National University, Seoul, Korea.
  • 3Department of Neuropsychiatry, Seoul National University Bundang Hospital, Seongnam, Kyunggi, Korea.
  • 4Neuroscience Research Institute of the Medical Research Center, Seoul National University, and Clinical Research Institute of Seoul National University Hospital, Seoul, Korea. jiwoomd@plaza.snu.ac.kr
  • 5Department of Neuropsychiatry, Kyunggi Provincial Hospital for Elderly, Yongin, Kyunggi, Korea.
  • 6Research division of Human Life Science, Seoul National University, Seoul, Korea.
  • 7Department of Neuropsychiatry, Seoul National University,College of Medicine and Seoul National University Hospital, Seoul, Korea.

Abstract

To examine whether the IL-1A(-889) polymorphism associates with a risk for Alzheimer's disease(AD) and acts interactively with the apolipoprotein(APOE) epsilon 4 in the development of AD, we performed genotype analyses of the IL-1A and the APOE of the 102 Korean AD patients and 200 Korean non-demented controls. We failed to detect a significant difference in genotypic and allelic frequencies of IL-1A between the AD group and control group. No overexpression of the IL-1A C/T genotype and IL-1A T allele was found when we analyzed the late-onset and early-onset patients, separately. There was no significant genetic interaction between IL-1A polymorphism and the APOE polymorphism. In conclusion, the IL-1A polymorphism did not contribute to the development of AD independently or interactively with the APOE epsilon4 allele in Koreans.

Keyword

Alzheimer's disease(AD); Interleukin-1A(IL-1A); Koreans; association

MeSH Terms

Alleles
Alzheimer Disease*
Apolipoproteins E
Asian Continental Ancestry Group
Genotype
Humans
Interleukins*
Polymorphism, Genetic*
Apolipoproteins E
Interleukins
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