Tumour necrosis factor-α gene polymorphisms and Alzheimer's disease

D Culpan; SH MacGowan; JM Ford; JAR Nicoll; WS Griffin; D Dewar; NJ Cairns; A Hughes; PG Kehoe; GK Wilcock

doi:10.1016/S0304-3940(03)00854-1

Tumour necrosis factor-α gene polymorphisms and Alzheimer's disease

D Culpan, SH MacGowan, JM Ford, JAR Nicoll, WS Griffin, D Dewar, NJ Cairns, A Hughes, PG Kehoe, GK Wilcock

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Abstract

Recent findings suggest that production of pro-inflammatory cytokines, such as tumour necrosis factor-alpha (TNF-α), is increased in the brains of people with Alzheimer's disease (AD). We used direct sequencing methods on a section of the enhancer/promoter region and on a smaller fragment located 10.5 kb upstream of the TNF-α gene to respectively examine TNF-α polymorphisms and TNF-a and -b microsatellite alleles in a cohort of 235 post-mortem confirmed AD and 130 control cases. None of the TNF-α point mutations or microsatellite alleles investigated proved to be independent risk factors for AD. However, when −308/A, −238/G and TNF-a2 were examined as a 2-1-2 haplotype, we observed that the absence of that haplotype was significantly associated with AD (P=0.014, Fisher's exact test) suggesting that the 2-1-2 haplotype may be protective against AD.

Translated title of the contribution	Tumour necrosis factor-α gene polymorphisms and Alzheimer's disease
Original language	English
Pages (from-to)	61 - 65
Number of pages	5
Journal	Neuroscience Letters
Volume	350 (1)
DOIs	https://doi.org/10.1016/S0304-3940(03)00854-1
Publication status	Published - 2003

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Publisher: Elsevier

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Cerebrovascular and Dementia Research Group

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title = "Tumour necrosis factor-α gene polymorphisms and Alzheimer's disease",

abstract = "Recent findings suggest that production of pro-inflammatory cytokines, such as tumour necrosis factor-alpha (TNF-α), is increased in the brains of people with Alzheimer's disease (AD). We used direct sequencing methods on a section of the enhancer/promoter region and on a smaller fragment located 10.5 kb upstream of the TNF-α gene to respectively examine TNF-α polymorphisms and TNF-a and -b microsatellite alleles in a cohort of 235 post-mortem confirmed AD and 130 control cases. None of the TNF-α point mutations or microsatellite alleles investigated proved to be independent risk factors for AD. However, when −308/A, −238/G and TNF-a2 were examined as a 2-1-2 haplotype, we observed that the absence of that haplotype was significantly associated with AD (P=0.014, Fisher's exact test) suggesting that the 2-1-2 haplotype may be protective against AD.",

author = "D Culpan and SH MacGowan and JM Ford and JAR Nicoll and WS Griffin and D Dewar and NJ Cairns and A Hughes and PG Kehoe and GK Wilcock",

note = "Publisher: Elsevier",

year = "2003",

doi = "10.1016/S0304-3940(03)00854-1",

language = "English",

volume = "350 (1)",

pages = "61 -- 65",

journal = "Neuroscience Letters",

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TY - JOUR

T1 - Tumour necrosis factor-α gene polymorphisms and Alzheimer's disease

AU - Culpan, D

AU - MacGowan, SH

AU - Ford, JM

AU - Nicoll, JAR

AU - Griffin, WS

AU - Dewar, D

AU - Cairns, NJ

AU - Hughes, A

AU - Kehoe, PG

AU - Wilcock, GK

N1 - Publisher: Elsevier

PY - 2003

Y1 - 2003

N2 - Recent findings suggest that production of pro-inflammatory cytokines, such as tumour necrosis factor-alpha (TNF-α), is increased in the brains of people with Alzheimer's disease (AD). We used direct sequencing methods on a section of the enhancer/promoter region and on a smaller fragment located 10.5 kb upstream of the TNF-α gene to respectively examine TNF-α polymorphisms and TNF-a and -b microsatellite alleles in a cohort of 235 post-mortem confirmed AD and 130 control cases. None of the TNF-α point mutations or microsatellite alleles investigated proved to be independent risk factors for AD. However, when −308/A, −238/G and TNF-a2 were examined as a 2-1-2 haplotype, we observed that the absence of that haplotype was significantly associated with AD (P=0.014, Fisher's exact test) suggesting that the 2-1-2 haplotype may be protective against AD.

AB - Recent findings suggest that production of pro-inflammatory cytokines, such as tumour necrosis factor-alpha (TNF-α), is increased in the brains of people with Alzheimer's disease (AD). We used direct sequencing methods on a section of the enhancer/promoter region and on a smaller fragment located 10.5 kb upstream of the TNF-α gene to respectively examine TNF-α polymorphisms and TNF-a and -b microsatellite alleles in a cohort of 235 post-mortem confirmed AD and 130 control cases. None of the TNF-α point mutations or microsatellite alleles investigated proved to be independent risk factors for AD. However, when −308/A, −238/G and TNF-a2 were examined as a 2-1-2 haplotype, we observed that the absence of that haplotype was significantly associated with AD (P=0.014, Fisher's exact test) suggesting that the 2-1-2 haplotype may be protective against AD.

U2 - 10.1016/S0304-3940(03)00854-1

DO - 10.1016/S0304-3940(03)00854-1

M3 - Article (Academic Journal)

SN - 1872-7972

VL - 350 (1)

SP - 61

EP - 65

JO - Neuroscience Letters

JF - Neuroscience Letters

ER -

Tumour necrosis factor-α gene polymorphisms and Alzheimer's disease

Abstract

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