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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >No association between polymorphisms in the lectin-like oxidised low density lipoprotein receptor (ORL1) gene on chromosome 12 and Alzheimer's disease in a UK cohort.
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No association between polymorphisms in the lectin-like oxidised low density lipoprotein receptor (ORL1) gene on chromosome 12 and Alzheimer's disease in a UK cohort.

机译:在英国队列中,第12号染色体上的凝集素样氧化低密度脂蛋白受体(ORL1)基因多态性与阿尔茨海默氏病之间没有关联。

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摘要

Genome scans in sporadic Alzheimer's disease (AD) have revealed possible susceptibility loci on chromosome 12. Recently, two studies were published investigating the +1071 and +1073 polymorphisms in the lectin-like oxidised low density lipoprotein receptor (OLR1) gene with AD, a gene that lies within the area of chromosome 12 linkage. OLR1 is a good candidate gene, due to its function in lipid metabolism pathways, other components of which have been previously implicated as risk factors for AD. We undertook an association study in our UK cohort of 356 AD patients and 358 matched controls, using the same polymorphisms and performing the same sub-group and haplotype analysis as previously described. We found no association with AD in our case-control group as a whole, or when stratified into those with early (<65 years) or late (>65 years) onset. When the group was split into APOE 4 bearers and 4 non-bearers, we could not confirm the associations described in the original study. Similarly, no significantdifferences were observed between AD patients and controls, in terms of their haplotype distributions. Therefore, in this present study, we find no evidence for the involvement of these ORL1 polymorphisms in increasing susceptibility to AD.
机译:偶发性阿尔茨海默氏病(AD)的基因组扫描已揭示12号染色体上可能的易感基因座。最近,发表了两项研究,研究了AD导致凝集素样氧化低密度脂蛋白受体(OLR1)基因中+1071和+1073多态性。位于12号染色体连锁区域内的基因。由于OLR1在脂类代谢途径中的功能,OLR1是一个很好的候选基因,以前它的其他成分被认为是AD的危险因素。我们在英国队列的356位AD患者和358位匹配的对照组中进行了一项关联研究,使用相同的多态性并进行了与先前所述相同的亚组和单倍型分析。整个病例对照组,或分层为发病早(<65岁)或晚期(> 65岁)的患者,我们均未发现与AD相关。当该小组分为APOE 4个承担者和4个非承担者时,我们无法确认原始研究中描述的关联。类似地,就单倍型分布而言,在AD患者和对照之间没有观察到显着差异。因此,在本研究中,我们没有发现这些ORL1多态性与AD易感性增加有关的证据。

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