A genetic variation of the inflammatory cytokine interleukin-6 delays the initial onset and reduces the risk for sporadic Alzheimer's disease

Ann Neurol. 1999 May;45(5):666-8. doi: 10.1002/1531-8249(199905)45:5<666::aid-ana18>3.0.co;2-3.


Local inflammatory processes surrounding the amyloid plaques contribute to the progression and acceleration of the Alzheimer's disease (AD)-related neurodegeneration. Interleukin-6 (IL-6) is an inflammatory cytokine with possible involvement in the local immune response occurring in the central nervous system of AD patients. We tested the hypothesis as to whether a genetic polymorphism of the IL-6 gene (IL-6) modifies the age at onset and risk for sporadic AD. Our results support an association of the C allele of the IL-6 genotype with a delayed initial onset and reduced disease risk and indicate that genetically determined alterations of the immune response may modify the course of AD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age of Onset
  • Aged
  • Aged, 80 and over
  • Alleles
  • Alzheimer Disease / genetics*
  • Alzheimer Disease / physiopathology
  • Alzheimer Disease / therapy*
  • Genetic Variation / genetics*
  • Humans
  • Interleukin-6 / therapeutic use*
  • Middle Aged
  • Polymorphism, Genetic / genetics
  • Risk Factors
  • Time Factors


  • Interleukin-6