Interleukin-6 promoter polymorphism: risk and pathology of Alzheimer's disease

被引:29
作者
Zhang, Y
Hayes, A
Pritchard, A
Thaker, U
Haque, MS
Lemmon, H
Harris, J
Cumming, A
Lambert, JC
Chartier-Harlin, MC
St Clair, D
Iwatsubo, T
Mann, DM
Lendon, CL [1 ]
机构
[1] Univ Birmingham, Queen Elizabeth Psychiat Hosp, Dept Psychiat, Birmingham B15 2QZ, W Midlands, England
[2] Hope Hosp, Greater Manchester Neurosci Ctr, Salford M6 8HD, Lancs, England
[3] Univ Aberdeen, Dept Mental Hlth, Aberdeen AB25 2ZD, Scotland
[4] Inst Pasteur, INSERM, U508, F-59019 Lille, France
[5] Univ Tokyo, Grad Sch Pharmaceut Sci, Dept Neuropathol & Neurosci, Tokyo, Japan
关键词
Alzheimer's disease; polymorphism; interleukin-6; promoter; brain; amyloid load; microglial cell load; reactive astrocytes;
D O I
10.1016/j.neulet.2004.03.008
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Inflammatory and immune responses are involved in the pathogenesis of Alzheimer's disease (AD). Interleukin-6 (IL-6), an inflammatory cytokine, is thought to play a role in neurodegeneration of the central nervous system and has been associated with increased amyloid precursor protein expression in vitro and greater cognitive decline. Previously a C - 174G polymorphism in the promoter of IL-6, which influences expression in vitro, has been found associated in some studies but not all. We investigated this polymorphism in a large independent UK sample of AD cases (n = 356) and controls (n = 434) but found no association. We extended the study to genotype/phenotype correlations but found no correlation with age of onset (it = 338), brain amyloid load (it = 126) or Tau load (17 101), brain microglial cell load (n = 65) or brain reactive astrocytes (n = 127). Our data do not support a pathogenic role in AD for the C 174G polymorphism in isolation. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:99 / 102
页数:4
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