An interleukin-6 promoter variant is not associated with an increased risk for Alzheimer's disease.
Recent studies have implicated interleukin-6 (IL-6) in the pathogenesis of Alzheimer's disease (AD). Neuro-inflammatory processes surrounding the amyloid plaques contribute to the progression of AD-related neurodegeneration. IL-6 is a multifunctional inflammatory cytokine which possibly acts as a mediator in the local immune response in the brain of AD patients. In this study we investigated whether the risk of developing AD is altered in carriers of the C allele of a G/C polymorphism at position -174. 113 AD patients and 108 age- and gender-matched nondemented control subjects were analysed. Genotyping of IL-6 was performed using standard PCR and restriction fragment length polymorphism methods. The results were adjusted for age, gender and apolipoprotein E epsilon4 status. There was no evidence for an association between the polymorphism and the risk of developing AD. No evidence of an earlier age at onset for carriers of the C allele was evaluated. We conclude that IL-6 (-174) polymorphism does not influence the risk of developing AD in our cohort.
Depboylu
Candan
C
Department of Neurology, Rheinische Friedrich-Wilhelms University Bonn, Bonn, Germany.
Lohmüller
Frank
F
Gocke
Petra
P
Du
Yansheng
Y
Zimmer
Reinhilde
R
Gasser
Thomas
T
Klockgether
Thomas
T
Dodel
Richard C
RC
D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D000544:Alzheimer Disease / Q000235:genetics*; D001057:Apolipoproteins E / Q000235:genetics; D015331:Cohort Studies; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006579:Heterozygote; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D017354:Point Mutation / Q000502:physiology; D012150:Polymorphism, Restriction Fragment Length; D011401:Promoter Regions, Genetic / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction
D001057:Apolipoproteins E; D015850:Interleukin-6