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DNA Repair Genes in Parkinson's Disease

机译：在帕金森病DNA修复基因

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Aims: There is a growing interest in the understanding of a possible role of DNA repair systems in ageing and neurodegenerative diseases after DNA damage is observed in the brain of individuals affected by neurode-generative diseases. In the light of these findings, we investigated whether DNA repair gene polymorphisms (XRCC1 Arg399G1n, XRCC3 Thr241Met XPD Lys751G1n, XPG Asp1104His, APE1 Asp148G1u, and HOGG1 Ser326Cys) account for an increased risk of Parkinson's disease (PD). Methods: The present analyses are based on 60 case subjects with PD and 108 unrelated healthy controls. Genotyping of DNA repair gene polymorphisms were detected by polymerase chain reaction–restriction fragment length polymorphism. Results: We, for the first time, demonstrated the positive association of APE', XRCC1, and XRCC3 DNA repair gene variants with PD risk. In our study, the frequencies of Glu/Glu genotype in APE1, Gin + genotype of XRCC1, and Thr + genotype of XRCC3 are higher in patients than in controls (p = 0.028, p = 0.002 and p = 0.046, respectively). Conclusions: In conclusion, our findings have suggested that APE', XRCC1, and XRCC3 genetic variants may be a risk factor by increasing oxidative stress that might cause the loss of dopaminergic cells in the substantiata nigra and locus caeruleus, leading to abnormal signal transmittion, and ultimately, the development of PD. In addition, gen-eration of reactive oxygen species from dopamine might affect the other DNA repair pathway proteins that we did not examine in the current study. Further studies with larger sample groups are necessary to clarify the role of DNA repair genes and the development of PD.
机译：目的:越来越多的兴趣的理解可能的DNA修复的作用系统在衰老和神经退行性疾病DNA损伤后大脑中观察到的个人受neurode-generative疾病。调查是否DNA修复基因, XRCC3多态性(XRCC1 Arg399G1n Thr241Met和HOGG1 Ser326Cys)占增加帕金森病(PD)的风险。目前的分析是基于60例受试者与PD和108年健康对照组无关。基因分型DNA修复基因的多态性检测到聚合酶链reaction-restriction片段长度多态性。第一次展示了积极的一面XRCC1猿”协会,XRCC3 DNA修复基因变异与帕金森病的风险。频率的Glu / Glu APE1基因型,杜松子酒+XRCC1基因型,用力推+ XRCC3基因型病人比对照组高(p =0.028, p = 0.002, p = 0.046)。结论:总之,我们的研究结果建议猿”,XRCC1, XRCC3基因通过增加变异可能是一个危险因素氧化应激可能造成的损失多巴胺能细胞substantiata黑质和轨迹山雀,导致异常信号transmittion,最终的发展PD。物种从多巴胺可能影响其他的DNA我们没有检查修复通路蛋白在当前的研究中。样本组是必要的澄清作用DNA修复基因和PD的发展。

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