...
首页> 外文期刊>The European Journal of Neuroscience >A polymorphism in lipoprotein lipase affects the severity of Alzheimer's disease pathophysiology.
【24h】

A polymorphism in lipoprotein lipase affects the severity of Alzheimer's disease pathophysiology.

机译:脂蛋白脂肪酶的多态性影响阿尔茨海默氏病病理生理的严重程度。

获取原文
获取原文并翻译 | 示例
           

摘要

Emerging evidences indicate a role for lipoprotein lipase (LPL) in degenerative states. Genetic variations in the LPL gene were previously associated to lipid imbalance and coronary artery disease (CAD) risk and severity, a condition that shares pathological features with common Alzheimer's disease (AD). To evaluate whether these genetic variations associate with the risk and pathophysiology of common AD, autopsy-confirmed patients (242 controls, 153 AD) were genotyped for a PvuII single nucleotide polymorphism (SNP; rs285; referred to as the P+ allele) of LPL. Brain LPL mRNA levels, cholesterol levels, amyloid concentration, senile plaques and neurofibrillary tangles density counts were measured and contrasted with specific LPL genotypes. When adjusted for age and sex, homozygosity for the P+ allele resulted in an odds ratio of 2.3 for the risk of developing AD. More importantly, we report that the presence of the P+ allele of LPL significantly affects its mRNA expression level (n = 51; P = 0.026), brain tissue cholesterol levels (n = 55; P = 0.0013), neurofibrillary tangles (n = 52; P = 0.025) and senile plaque (n 52; P polymorphism in the lipoprotein lipase gene modulates the risk level for sporadic AD in the eastern Canadian population but more importantly, indirectly modulates the pathophysiology of the brain in autopsy-confirmed cases.
机译:新兴证据表明脂蛋白脂肪酶(LPL)在退化状态中的作用。 LPL基因的遗传变异先前与脂质失衡和冠状动脉疾病(CAD)的风险和严重程度有关,这种疾病与常见的阿尔茨海默氏病(AD)具有病理特征。为了评估这些遗传变异是否与常见AD的风险和病理生理有关,对尸检确诊的患者(242名对照,153 AD)进行了LPL的PvuII单核苷酸多态性(SNP; rs285;称为P +等位基因)基因分型。测量大脑LPL mRNA水平,胆固醇水平,淀粉样蛋白浓度,老年斑和神经原纤维缠结密度计数,并与特定LPL基因型进行对比。调整了年龄和性别后,P +等位基因的纯合性导致罹患AD的风险比值比为2.3。更重要的是,我们报告LPL的P +等位基因的存在显着影响其mRNA表达水平(n = 51; P = 0.026),脑组织胆固醇水平(n = 55; P = 0.0013),神经原纤维缠结(n = 52 ; P = 0.025)和老年斑(n 52;脂蛋白脂肪酶基因中的P多态性可调节加拿大东部人群散发性AD的风险水平,但更重要的是,间接可调节尸检确诊病例的大脑病理生理。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号