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首页> 外文期刊>Neurobiology of Aging: Experimental and Clinical Research >An exploratory analysis on gene-environment interactions for Parkinson disease
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An exploratory analysis on gene-environment interactions for Parkinson disease

机译:帕金森病基因与环境相互作用的探索性分析

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Little is known about gene-environment interactions in Parkinson disease (PD). We examined potential interactions of smoking and caffeine intake with 10 genome-wide association studies single nucleotide polymorphisms (SNPs) at or near the SNCA, MAPT, LRRK2, and HLA loci among 584 PD patients and 1571 controls. The main effects of these SNPs and environmental exposures were consistent with previous reports. Family history of PD was associated with PD risk (odds ratio = 2.71, 95% confidence interval, 1.97-3.74), which was little affected by further adjustment for these SNPs and environmental exposures. Overall, we did not find significant interactions of either smoking or caffeine intake with these SNPs. However, with a combined smoking and caffeine intake exposure, we found a significant interaction with rs2896905 at SLC2A13, near LRRK2 (p uncorrected = 0.0008). Each A allele was associated with a 35% higher PD risk among never smokers with low caffeine intake, but with a 32% lower risk among smokers with high caffeine intake. This study provides preliminary evidence of a potential gene-environment interaction for PD, which should be investigated in future studies. Published by Elsevier Inc.
机译:关于帕金森病(PD)中的基因-环境相互作用知之甚少。我们通过584名PD患者和1571名对照的SNCA,MAPT,LRRK2和HLA基因座或附近的10个全基因组关联研究,研究了吸烟和摄入咖啡因的潜在相互作用。这些SNP和环境暴露的主要影响与以前的报告一致。 PD家族史与PD风险相关(几率= 2.71,95%置信区间为1.97-3.74),而这些SNP和环境暴露的进一步调整对其影响很小。总体而言,我们未发现吸烟或咖啡因摄入与这些SNP有显着的相互作用。然而,结合吸烟和咖啡因摄入暴露,我们发现LRRK2附近的SLC2A13与rs2896905有显着相互作用(p未校正= 0.0008)。在从未摄入咖啡因的吸烟者中,每个A等位基因的PD风险高35%,但是在摄入咖啡因高的吸烟者中,PD风险低32%。这项研究提供了PD潜在的基因-环境相互作用的初步证据,应在以后的研究中进行研究。由Elsevier Inc.发布

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