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

被引：61

作者：

Culpan, D

MacGowan, SH

Ford, JM

Nicoll, JAR

Griffin, WS

Dewar, D

Cairns, NJ

Hughes, A

Kehoe, PG

Wilcock, GK

机构：

[1] Univ Bristol, Frenchay Hosp, Dept Care Elderly, Bristol BS16 1LE, Avon, England

[2] Univ Southampton, Div Clin Neurosci, Southampton, Hants, England

[3] Univ Arkansas Med Sci, Donald W Reynolds Dept Genet Med & Physiol, Dept Vet Affairs Med Ctr, Little Rock, AR 72205 USA

[4] Univ Glasgow, Wellcome Surg Unit, Glasgow, Lanark, Scotland

[5] Univ London Kings Coll, Inst Psychiat, Dept Neuropathol, London SE5 8NW, England

来源：

NEUROSCIENCE LETTERS | 2003年 / 350卷 / 01期

关键词：

Alzheimer's disease; tumour necrosis factor-alpha; polymorphisms; HLA-DRB1*03;

D O I：

10.1016/S0304-3940(03)00854-1

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Recent findings suggest that production of pro-inflammatory cytokines, such as tumour necrosis factor-alpha (TNF-alpha), 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-alpha gene to respectively examine TNF-alpha 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-alpha 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. (C) 2003 Elsevier Ireland Ltd. All rights reserved.

引用

页码：61 / 65

页数：5

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