Potential mechanisms for low uric acid in Parkinson disease

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• 作者：Radhika Sampat ; Sarah Young ; Ami Rosen ; Douglas Bernhard…
• 关键词：Uric acid ; Allantoin ; Oxidative stress ; Metabolism ; Parkinson disease
• 刊名：Journal of Neural Transmission
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：123
• 期：4
• 页码：365-370
• 全文大小：427 KB
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• 作者单位：Radhika Sampat (1)
  Sarah Young (2)
  Ami Rosen (1)
  Douglas Bernhard (1)
  David Millington (2)
  Stewart Factor (1)
  H. A. Jinnah (1) (3)
  
  1. Department of Neurology, Emory University, Atlanta, GA, 30322, USA
  2. Department of Biochemistry, Duke University, Durham, NC, 27713, USA
  3. Department of Human Genetics and Pediatrics, Emory University, Suite 6300 Woodruff Memorial Building, 101 Woodruff Circle, Atlanta, GA, 30322, USA
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Neurology
  Pharmacology and Toxicology
  Psychiatry
  
• 出版者：Springer Wien
• ISSN：1435-1463

文摘

Several epidemiologic studies have described an association between low serum uric acid (UA) and Parkinson disease (PD). Uric acid is a known antioxidant, and one proposed mechanism of neurodegeneration in PD is oxidative damage of dopamine neurons. However, other complex metabolic pathways may contribute. The purpose of this study is to elucidate potential mechanisms of low serum UA in PD. Subjects who met diagnostic criteria for definite or probable PD (n = 20) and controls (n = 20) aged 55–80 years were recruited. Twenty-four hour urine samples were collected from all participants, and both uric acid and allantoin were measured and corrected for body mass index (BMI). Urinary metabolites were compared using a twoway ANOVA with diagnosis and sex as the explanatory variables. There were no significant differences between PD and controls for total UA (p = 0.60), UA corrected for BMI (p = 0.37), or in the interaction of diagnosis and sex on UA (p = 0.24). Similarly, there were no significant differences between PD and controls for allantoin (p = 0.47), allantoin corrected for BMI (p = 0.57), or in the interaction of diagnosis and sex on allantoin (p = 0.78). Allantoin/UA ratios also did not significantly differ by diagnosis (p = 0.99). Our results imply that low serum UA in PD may be due to an intrinsic mechanism that alters the homeostatic set point for serum UA in PD, and may contribute to relatively lower protection against oxidative damage. These findings provide indirect support for neuroprotection trials aimed at raising serum UA.