+874(T→A) single nucleotide gene polymorphism does not represent a risk factor for Alzheimer's disease

被引:5
|
作者
Galimberti L. [1 ]
Arosio B. [1 ]
Calabresi C. [1 ]
Scurati S. [1 ]
Hamilton S. [1 ]
Delli Carpini S. [1 ]
Vergani C. [1 ]
Annoni G. [2 ]
机构
[1] Department of Geriatrics, Ospedale Maggiore IRCCS, University of Milano, Milan
[2] Department of Clinical Medicine, Prevention and Medical Biotechnology, University of Milano-Bicocca, Milano
关键词
Alzheimer Disease; Alzheimer Disease Patient; Single Nucleotide Polymorphism; Single Nucleotide Gene Polymorphism; Cytokine Class;
D O I
10.1186/1742-4933-1-6
中图分类号
学科分类号
摘要
In the recent years, several cytokines have been associated with Alzheimer's disease (AD) development and progression and many studies have correlated this risk with polymorphisms in the genes encoding these molecules. Also the type 1 cytokine interferon (IFN)-γ belongs to a cytokine class that affects the immune function; in fact it plays a major role in defence against viruses and intracellular pathogens but also in the induction of the immune-mediated inflammatory response. The aim of this study was to evaluate the role of IFN-γ in AD by studying the association of +874T→ IFN-γ gene polymorphism with AD. We included in this study 115 AD patients (70 women, 45 men, mean age 80) and 90 sex and age-matched healthy controls (HC, 51 women, 39 men, mean age 82) from northern Italy. Genomic DNA was extracted with the salting-out method from whole blood of all subjects; the genotyping at IFN-γ loci was assessed with ARMS-PCR. The data obtained from the +874T→ IFN-γ gene polymorphism analysis of AD patients and HC lack of any statistically significant differences also when stratified according to gender. In conclusion these results confirm the previous shown lack of association between +874T→ IFN-γ gene polymorphism and the risk of AD. However, other polymorphisms have been demonstrated to influence IFN-γ transcription and since natural killer cells of AD patients show higher production of the cytokine, further analysis will be necessary to clarify the role of this gene in the pathogenesis. of the disease. © 2004 Galimberti et al; licensee BioMed Central Ltd.
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