Northern Chinese Han populations with sporadic Alzheimer’s disease and the role of urokinase-type plasminogen activator gene promoter polymorphisms  

作　　者：Di Han Yan Wang Hongyun Li Jianping Jia 

机构地区：[1]Department of Emergency Neurology, Medical School Hospital of Qingdao University, Qingdao 266003, Shandong Province, China [2]Department of Neurology, Medical School Hospital of Qingdao University, Qingdao 266003, Shandong Province, China [3]Department of Neurology, Xuanwu Hospital of the Capital Medical University, Beijing 100053, China

出　　处：《Neural Regeneration Research》2010年第2期150-155,共6页中国神经再生研究（英文版）

基　　金：the National Key Technology R&D Program in the Eleventh Five-year Plan Period,No.2006BAI02B01;the National Basic Research 973 Program,No.2006CB500700;the Beijing Natural Science Foundation,No.7071004;Funding Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality

摘　　要：BACKGROUND; Polymorphisms of urokinase-type plasminogen activator gene （PLAU） have recently been reported to be associated with sporadic Alzheimer＇ disease （SAD）. However, most studies have focused on the exon region of this gene, and there is no report on the association between promoter polymorphisms of the PLAU and SAD. OBJECTIVE： To determine whether SAD is associated with promoter polymorphisms of PLAU in Northem Han Chinese. DESIGN, TIME AND SETTING： A case-control study was performed at Neurology Laboratory of Xuanwu Hospital of the Capital Medical University from September 2006 to July 2008. PARTICIPANTS： A total of 397 participants living in Beijing were assigned to SAD [n = 196, including 103 males and 93 females, mean age of （64 ± 7） years] and control [n = 201, including 108 males and 93 females, mean age of （68 ± 6） years] groups. The patients were diagnosed and met the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer＇s Disease and Related Disorder Association criteria for possible Alzheimer＇s disease. Controls received clinical, mental, and neurological examinations to rule out cognitive deficiencies. All controls had Mini-Mental Status Examination scores 〉 27. METHODS： Genotypes of PLAU and apolipoprotein-E were examined in 196 patients with SAD and 201 age- and sex-matched controls from the same community using polymerase chain reaction-restriction fragment length polymorphism method. SPSS 11.5 software was used for data analysis, distribution of allele and genotypic frequency were calculated, and Hardy-Weinberg was also performed in this study. MAIN OUTCOME MEASURES： The main outcome measures were allele and genotype frequency differences in the promoter region of the PLAU gene between SAD and control subjects. RESULTS： In Chinese Han populations, the two polymorphisms in PLAU promoter were -25 C/T （rs2227579） and 43 G/T （rs2227580）. Detection of these promoter polymorphisms revealed significant differences in alleleBACKGROUND; Polymorphisms of urokinase-type plasminogen activator gene （PLAU） have recently been reported to be associated with sporadic Alzheimer＇ disease （SAD）. However, most studies have focused on the exon region of this gene, and there is no report on the association between promoter polymorphisms of the PLAU and SAD. OBJECTIVE： To determine whether SAD is associated with promoter polymorphisms of PLAU in Northem Han Chinese. DESIGN, TIME AND SETTING： A case-control study was performed at Neurology Laboratory of Xuanwu Hospital of the Capital Medical University from September 2006 to July 2008. PARTICIPANTS： A total of 397 participants living in Beijing were assigned to SAD [n = 196, including 103 males and 93 females, mean age of （64 ± 7） years] and control [n = 201, including 108 males and 93 females, mean age of （68 ± 6） years] groups. The patients were diagnosed and met the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer＇s Disease and Related Disorder Association criteria for possible Alzheimer＇s disease. Controls received clinical, mental, and neurological examinations to rule out cognitive deficiencies. All controls had Mini-Mental Status Examination scores 〉 27. METHODS： Genotypes of PLAU and apolipoprotein-E were examined in 196 patients with SAD and 201 age- and sex-matched controls from the same community using polymerase chain reaction-restriction fragment length polymorphism method. SPSS 11.5 software was used for data analysis, distribution of allele and genotypic frequency were calculated, and Hardy-Weinberg was also performed in this study. MAIN OUTCOME MEASURES： The main outcome measures were allele and genotype frequency differences in the promoter region of the PLAU gene between SAD and control subjects. RESULTS： In Chinese Han populations, the two polymorphisms in PLAU promoter were -25 C/T （rs2227579） and 43 G/T （rs2227580）. Detection of these promoter polymorphisms revealed significant differences in allele

关 键 词：PLAU gene PROMOTER Alzheimer＇s disease POLYMORPHISM 

分 类 号：R[医药卫生]