载脂蛋白A-Ⅳ基因360位点与阿尔茨海默病和帕金森病的关系研究

Study of the Association of Apolipoprotein A-Ⅳ Codon 360 Mutation with Alzheimer and Parkinson Diseases

目的 探讨载脂蛋白 A- (apolipoprotein A- ,Apo A- )基因 3 60位点多态性和血脂指标与阿尔茨海默病 (Alzheimer disease,AD)和帕金森病 (Parkinson disease,PD)的关系。方法 应用存在特异性引物的简便、直接的聚合酶链反应 (PCR)方法 ,检测具有临床诊断证据的 3 9例 AD患者 [(77.7± 8.1 )岁 ]、3 6例 PD患者[(74.8± 1 0 .0 )岁 ]和 2 0 8名健康人 [(5 4.3± 1 1 .2 )岁 ]Apo A- 基因 3 60位点 (Gln/His)的突变 ,同时应用常规临床化学方法检测上述人群的血清总胆固醇 (TC)、甘油三酯 (TG)和高密度脂蛋白胆固醇 (HDL-C)水平。结果 在所有患者和健康人群中 ,均未发现 Apo A- 3 60 His等位基因携带者 ;两个病患组与对照组血清 TC和HDL-C水平差异无显著性 ,但病患组血清 TG水平却显著高于对照组 (P <0 .0 5 ) ;PD组血清 TG水平显著高于 AD组 (P <0 .0 5 )。结论 此研究未发现 Apo A- 基因 3 60位点突变基因型携带者 ,故无法探讨其与 AD和PD的关系 ;血脂水平与 AD和

Objective To investigate the possible association of the apolipoprotein A Ⅳ (ApoA Ⅳ) gene codon 360 mutation and serum lipid traits with Alzheimer disease (AD) and Parkinson disease (PD).Methods A simple and direct polymerase chain reaction of genotyping ApoA Ⅳ codon 360 mutation with specific primers was applied to determine the genotype of ApoA Ⅳ at codon 360 in the population samples of 39 AD[(77 7±[JP2]8 1)years] and 36 PD and 36 PD [(74 8±10 0) years] patients as well as the matched 208 healthy controls [(54 3±11 2)[JP]years]. Routine clinical chemistry methods for determining the level of total cholesterol (TC), triglyceride (TG) and high density lipoprotein cholesterol (HDL C) were used to measure the individual serum parameters.. Routine clinical chemistry methods for determining the level of total cholesterol (TC), triglyceride (TG) and high density lipoprotein cholesterol (HDL C) were used to measure the individual serum parameters.Results No mutant allele of the ApoA Ⅳ gene 360 codon was found among all the studied subjects. Mean value of serum TC and HDL C concentrations were not significantly different among these three groups, but serum TG concentration in the case groups was significantly increased in the cases with the PD patients with thehighestmeanvalue (P<0 05).Conclusions SincethemutantalleleoftheApoA Ⅳgene360 codon was not found in the studied population, it suggested that this loci could not be used to study the association of ApoA Ⅳ codon 360 with AD and PD. Further study by extending the sample size is needed to verify the association of serum lipid and lipoprotein levels with the development of neurodegerative disease, such as AD and PD.