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

Y  Zhang; A  Hayes; A  Pritchard; U  Thaker; M S  Haque; H  Lemmon; J  Harris; A  Cumming; J C  Lambert; M C  Chartier-Harlin; D  St Clair; T  Iwatsubo; D M  Mann; C L  Lendon

doi:10.1016/j.neulet.2004.03.008

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

Y Zhang, A Hayes, A Pritchard, U Thaker, M S Haque, H Lemmon, J Harris, A Cumming, J C Lambert, M C Chartier-Harlin, D St Clair, T Iwatsubo, D M Mann, C L Lendon

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Abstract

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.

Original language	English
Pages (from-to)	99-102
Number of pages	4
Journal	Neuroscience Letters
Volume	362
Issue number	2
Early online date	16 Apr 2004
DOIs	https://doi.org/10.1016/j.neulet.2004.03.008
Publication status	Published - 20 May 2004

Keywords

Alzheimer's disease
polymorphism
interleukin-6
promoter
brain
amyloid load
microglial cell load
reactive astrocytes
genetic polymorphisms
association
Beta
population
protein

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10.1016/j.neulet.2004.03.008

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title = "Interleukin-6 promoter polymorphism: risk and pathology of Alzheimer's disease",

abstract = "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.",

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author = "Y Zhang and A Hayes and A Pritchard and U Thaker and Haque, {M S} and H Lemmon and J Harris and A Cumming and Lambert, {J C} and Chartier-Harlin, {M C} and {St Clair}, D and T Iwatsubo and Mann, {D M} and Lendon, {C L}",

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AU - Zhang, Y

AU - Hayes, A

AU - Pritchard, A

AU - Thaker, U

AU - Haque, M S

AU - Lemmon, H

AU - Harris, J

AU - Cumming, A

AU - Lambert, J C

AU - Chartier-Harlin, M C

AU - St Clair, D

AU - Iwatsubo, T

AU - Mann, D M

AU - Lendon, C L

PY - 2004/5/20

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N2 - 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.

AB - 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.

KW - Alzheimer's disease

KW - polymorphism

KW - interleukin-6

KW - promoter

KW - brain

KW - amyloid load

KW - microglial cell load

KW - reactive astrocytes

KW - genetic polymorphisms

KW - association

KW - Beta

KW - population

KW - protein

U2 - 10.1016/j.neulet.2004.03.008

DO - 10.1016/j.neulet.2004.03.008

M3 - Article

SN - 0304-3940

VL - 362

SP - 99

EP - 102

JO - Neuroscience Letters

JF - Neuroscience Letters

IS - 2

ER -

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

Abstract

Keywords

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