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本文引用的文献

1
Uric acid relates to dopamine transporter availability in Parkinson's disease.尿酸与帕金森病中多巴胺转运体的可用性有关。
Acta Neurol Scand. 2015 Feb;131(2):127-31. doi: 10.1111/ane.12295. Epub 2014 Oct 7.
2
Urate and neuroprotection trials.尿酸与神经保护试验。
Lancet Neurol. 2014 Aug;13(8):758. doi: 10.1016/S1474-4422(14)70138-3.
3
Urate in Parkinson's disease: more than a biomarker?帕金森病中的尿酸:不仅仅是生物标志物?
Curr Neurol Neurosci Rep. 2012 Aug;12(4):367-75. doi: 10.1007/s11910-012-0282-7.
4
Serum urate and probability of dopaminergic deficit in early "Parkinson's disease".血清尿酸与早期“帕金森病”多巴胺能缺陷的概率。
Mov Disord. 2011 Aug 15;26(10):1864-8. doi: 10.1002/mds.23741. Epub 2011 Apr 29.
5
Urate as a predictor of the rate of clinical decline in Parkinson disease.尿酸作为帕金森病临床衰退率的预测指标。
Arch Neurol. 2009 Dec;66(12):1460-8. doi: 10.1001/archneurol.2009.247.
6
Protein targets of oxidative damage in human neurodegenerative diseases with abnormal protein aggregates.人类神经退行性疾病中异常蛋白聚集的氧化损伤蛋白靶点。
Brain Pathol. 2010 Mar;20(2):281-97. doi: 10.1111/j.1750-3639.2009.00326.x. Epub 2009 Aug 6.
7
Uric acid: the oxidant-antioxidant paradox.尿酸:氧化-抗氧化悖论
Nucleosides Nucleotides Nucleic Acids. 2008 Jun;27(6):608-19. doi: 10.1080/15257770802138558.
8
Serum urate as a predictor of clinical and radiographic progression in Parkinson disease.血清尿酸作为帕金森病临床和影像学进展的预测指标。
Arch Neurol. 2008 Jun;65(6):716-23. doi: 10.1001/archneur.2008.65.6.nct70003. Epub 2008 Apr 14.
9
Glycolitic enzymes are targets of oxidation in aged human frontal cortex and oxidative damage of these proteins is increased in progressive supranuclear palsy.糖酵解酶是老年人类额叶皮质氧化的靶点,并且在进行性核上性麻痹中这些蛋白质的氧化损伤会增加。
J Neural Transm (Vienna). 2008;115(1):59-66. doi: 10.1007/s00702-007-0800-y. Epub 2007 Aug 21.
10
Plasma urate and risk of Parkinson's disease.血浆尿酸与帕金森病风险
Am J Epidemiol. 2007 Sep 1;166(5):561-7. doi: 10.1093/aje/kwm127. Epub 2007 Jun 20.

尿酸水平与进行性核上性麻痹之间的关系。

Relationship between uric acid levels and progressive supranuclear palsy.

作者信息

Brody David M, Litvan Irene, Warner Steve, Riley David E, Hall Deborah A, Kluger Benzi M, Shprecher David R, Cunningham Christopher R

机构信息

Movement Disorder Center, Department of Neurosciences, University of California San Diego, San Diego, California, USA.

Division of Movement Disorders, Department of Neurology, University of Louisville School of Medicine, Louisville, Kentucky, USA.

出版信息

Mov Disord. 2016 May;31(5):663-7. doi: 10.1002/mds.26535. Epub 2016 Feb 18.

DOI:10.1002/mds.26535
PMID:26890571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5258200/
Abstract

INTRODUCTION

The pathophysiology of both PD and PSP is characterized by a pro-oxidant state. Uric acid is an oxidative stress marker. High uric acid blood levels have been associated with a reduced risk of PD and a decreased rate of disease progression. We investigated whether a low serum concentration of uric acid is also associated with PSP.

METHODS

We measured serum uric acid concentrations in a subsample of the ENGENE PSP Cohort that included 75 cases and 75 frequency-matched-by-sex healthy controls (69 spouses, 6 in-laws) from four centers willing to participate (Case Western, Rush University, University of Utah, and University of Louisville). Case severity was characterized using the total PSP-Rating Scale, UPDRS, and Mattis Dementia Rating Scale. Unconditional logistic regression, Pearson's chi-squared test, and analysis of variance were used, as appropriate.

RESULTS

The mean uric acid level among cases (4.0 mg/dL) was not significantly lower than that of controls (4.1 mg/dL). When controlling for sex, there were no between-group statistical differences in uric acid levels. Uric acid levels were not correlated with disease severity.

CONCLUSIONS

The results of this study do not provide evidence of uric acid having a protective role in PSP, even if oxidative injury is important in the pathophysiology of this disorder. The lack of statistical significance suggests that there is no direct association between uric acid levels and PSP. However, a small inverse association cannot be excluded. © 2016 Movement Disorder Society.

摘要

引言

帕金森病(PD)和进行性核上性麻痹(PSP)的病理生理学特征均为促氧化状态。尿酸是一种氧化应激标志物。高血尿酸水平与PD风险降低及疾病进展速率减慢相关。我们研究了低血清尿酸浓度是否也与PSP有关。

方法

我们在ENGENE PSP队列的一个子样本中测量了血清尿酸浓度,该子样本包括来自四个愿意参与的中心(凯斯西储大学、拉什大学、犹他大学和路易斯维尔大学)的75例患者以及75名按性别频率匹配的健康对照者(69名配偶、6名姻亲)。使用PSP总评分量表、统一帕金森病评定量表(UPDRS)和马蒂斯痴呆评定量表来表征病例的严重程度。酌情使用无条件逻辑回归、Pearson卡方检验和方差分析。

结果

病例组的平均尿酸水平(4.0mg/dL)并不显著低于对照组(4.1mg/dL)。在控制性别后,尿酸水平在组间无统计学差异。尿酸水平与疾病严重程度无关。

结论

本研究结果未提供尿酸在PSP中具有保护作用的证据,即便氧化损伤在该疾病的病理生理学中很重要。缺乏统计学显著性表明尿酸水平与PSP之间无直接关联。然而,不能排除存在小的负相关。©2016运动障碍协会。