Association study of polymorphisms in the cyclooxygenase-2 gene and Alzheimer’s disease risk in Chinese
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  • 作者:Wenlu Tang (1)
    Meixia He (3)
    Bo Yang (3)
    Kankan Wei (4)
    Ming Yin (5)
    Lirong Zhang (2)
  • 关键词:Alzheimer’s disease ; Cyclooxygenase ; 2 ; Single nucleotide polymorphisms ; Susceptibility
  • 刊名:Neurological Sciences
  • 出版年:2013
  • 出版时间:May 2013
  • 年:2013
  • 卷:34
  • 期:5
  • 页码:695-699
  • 全文大小:167KB
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  • 作者单位:Wenlu Tang (1)
    Meixia He (3)
    Bo Yang (3)
    Kankan Wei (4)
    Ming Yin (5)
    Lirong Zhang (2)

    1. Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China
    3. Department of Pharmacology, Henan Academy of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, China
    4. Department of Pharmacy, The Fourth Affiliated Hospital, Zhengzhou University, Zhengzhou, China
    5. School of Pharmacy, Shanghai Jiao Tong University, Shanghai, 200240, China
    2. Department of Pharmacology, School of Medicine, Zhengzhou University, 100 Science Road, Zhengzhou, 450001, China
  • ISSN:1590-3478
文摘
To determine if polymorphisms (?65G/C, ?195G/A and 8473T/C) of the cyclooxygenase-2 (COX-2) gene can be associated with Alzheimer disease (AD). The frequency of the polymorphisms was determined in 244 cases and 226 controls. The results revealed that the distributions of COX-2 ?65G/C and 8473T/C polymorphisms were statistically not significant between AD cases and controls. The genotype distributions and allele frequencies of COX-2 ?195G/A polymorphism in the cases were statistically significantly different from the controls (P?<?0.05). The A/A distribution and A allele frequency were significantly lower in the AD group. COX-2 ?195AA carriers showed a one-third lower risk of developing AD as compared to those with ?195GG and GA genotypes (OR?=?0.3, 95?% CI 0.194-.465, P?=?0.000). This study suggested that ?195G/A polymorphism of the COX-2 gene is associated with the risk of AD, and the A allele represents a protective factor in patients with AD.
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