首页> 美国卫生研究院文献>Iranian Journal of Basic Medical Sciences >Ccr2-64i and Ccr5 Δ32 Polymorphisms in Patients with Late-Onset Alzheimer’s disease; A Study from Iran (Ccr2-64i And Ccr5 Δ32 Polymorphisms in Alzheimer’s disease)
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Ccr2-64i and Ccr5 Δ32 Polymorphisms in Patients with Late-Onset Alzheimer’s disease; A Study from Iran (Ccr2-64i And Ccr5 Δ32 Polymorphisms in Alzheimer’s disease)

机译:晚期阿尔茨海默氏病患者的Ccr2-64i和Ccr5Δ32多态性;伊朗的一项研究(阿尔茨海默氏病中Ccr2-64i和Ccr5Δ32多态性)

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摘要

>Objective(s):Alzheimer’s disease (AD) is a complex disease with multifactorial etiology. Inflammation has been proven to have an important role in the pathogenesis of AD. Both CCR2 and CCR5 genes expression increase in AD patients comparing to control subjects. CCR5 gene encodes a protein which is a member of the beta chemokine receptors family of integral membrane proteins. CCR5-Δ32 is a genetic variant of CCR5 and is characterized by the presence of a 32-bp deletion in the coding region of the gene, which leads to the expression of a nonfunctional receptor, and the CCR2-64I has a change of valine to isoleucine at codon 64, in the first transmembrane domain. It has been proved that both genes have important roles in different stages of inflammation. >Materials and Methods:The frequencies of CCR5∆32 and CCR2-64I variations were determined in 156 AD patients and 161 control subjects using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods, and the results were compared among AD and healthy controls. >Results >:Statistical analysis showed no significant difference in the distributions of CCR5∆32 and CCR2-64I between the AD patients and healthy controls (P> 0.05). Stratifying the samples by gender, genetic background and presence of ApoEε4 allele showed no significant effect on the distributions of CCR5∆32 and CCR2-64I (P> 0.05). >Conclusion:Our study did not show an association between CCR5∆32 and CCR2-64I variations and AD in the Iranian population. Further confirmatory studies with bigger number of samples are recommended.
机译:>目标:阿尔茨海默氏病(AD)是一种具有多种病因的复杂疾病。炎症已被证明在AD的发病机理中具有重要作用。与对照组相比,AD患者的CCR2和CCR5基因表达均增加。 CCR5基因编码一种蛋白质,该蛋白质是完整膜蛋白的β趋化因子受体家族的成员。 CCR5-Δ32是CCR5的遗传变异体,其特征在于在基因的编码区域中存在32bp的缺失,这导致了非功能性受体的表达,并且CCR2-64I具有缬氨酸的改变。在第一个跨膜结构域中,第64位密码子异亮氨酸。业已证明,这两种基因在炎症的不同阶段均具有重要作用。 >材料和方法:使用聚合酶链反应(PCR)和限制性片段长度多态性(RFLP)方法测定了156名AD患者和161名对照受试者的CCR5∆32和CCR2-64I变异频率,以及将结果与AD和健康对照进行比较。 >结果 >:S 统计分析显示,AD患者与健康对照组之间CCR5∆32和CCR2-64I的分布无显着差异(P> 0.05)。按性别,遗传背景和ApoEε4等位基因的存在对样本进行分层显示,对CCR5∆32和CCR2-64I的分布没有显着影响(P> 0.05)。 >结论:我们的研究没有显示CCR5∆32和CCR2-64I变异与伊朗人群的AD之间存在关联。建议使用更多样品进行进一步的验证性研究。

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