Potential mechanisms for low uric acid in Parkinson disease

• Authors: Radhika Sampat, Emory University; Sarah Young, Duke University; Ami Rosen, Emory University; Douglas Bernhard, Emory University; David Millington, Duke University; Stewart Factor, Emory University; Hyder A Jinnah, Emory University
• Journal Title: Journal of Neural Transmission
• Volume: Volume 123, Number 4
• Publisher: Springer Verlag (Germany) | 2016-04-01, Pages 365-370
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1007/s00702-015-1503-4
• Subjects: Biology, Neuroscience; Chemistry, Biochemistry; Health Sciences, Epidemiology
• Keywords: Science & Technology; Life Sciences & Biomedicine; Clinical Neurology; Neurosciences; Neurosciences & Neurology; Uric acid; Allantoin; Oxidative stress; Metabolism; Parkinson disease; SERUM URATE; OXIDATIVE STRESS; RISK; PROGRESSION; BIOMARKER; HUMANS

Abstract

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.