No genetic association between tumour necrosis factor receptor II 196R polymorphism and Japanese sporadic Alzheimer's disease

Psychiatr Genet. 2004 Mar;14(1):53-5. doi: 10.1097/00041444-200403000-00009.

Abstract

Recent studies have reported that acute effects of tumour necrosis factor (TNF), a pro-inflammatory cytokine, are limited by binding to a soluble receptor, TNF receptor II, and the G allele at position 196 in exon 6 of the TNF receptor II gene (TNFRII 196R) has been associated with auto-immune diseases. Since complex interactions among cytokines have been suggested around senile plaques in Alzheimer's disease, TNF might be associated with ageing and the pathophysiology of Alzheimer's disease. We examined the TNFRII 196R polymorphism in 243 Japanese sporadic Alzheimer's disease cases and 106 control cases using a polymerase chain reaction-restriction fragment length polymorphism method. Allelic frequencies with TNFRII 196R T/G polymorphism were 28.3% and 27.4% in the control and Alzheimer's disease groups, respectively. The results showed no genetic association between TNFRII 196R polymorphism and Alzheimer's disease. The TNFRII 196R G allele does not appear to be associated with Alzheimer's disease susceptibility in a Japanese population.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Age of Onset
  • Aged
  • Aged, 80 and over
  • Alzheimer Disease / epidemiology
  • Alzheimer Disease / genetics*
  • Amino Acid Substitution*
  • Antigens, CD / genetics*
  • Chromosomes, Human, Pair 1 / genetics
  • Exons / genetics
  • Female
  • Gene Frequency
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Japan / epidemiology
  • Male
  • Middle Aged
  • Polymorphism, Single Nucleotide*
  • Receptors, Tumor Necrosis Factor / genetics*
  • Receptors, Tumor Necrosis Factor, Type II

Substances

  • Antigens, CD
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Type II