David M Brody1, Irene Litvan1,2, Steve Warner, David E Riley3, Deborah A Hall4, Benzi M Kluger5, David R Shprecher6, Christopher R Cunningham2. 1. Movement Disorder Center, Department of Neurosciences, University of California San Diego, San Diego, California, USA. 2. Division of Movement Disorders, Department of Neurology, University of Louisville School of Medicine, Louisville, Kentucky, USA. 3. InMotion, Warrensville Heights, Ohio, USA. 4. Department of Neurology, Rush University Medical Center, Chicago, Illinois, USA. 5. Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA. 6. Department of Neurology, University of Utah, Salt City, Utah, USA.
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.
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 ENGENEPSP 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.
Authors: Michael A Schwarzschild; Kenneth Marek; Shirley Eberly; David Oakes; Ira Shoulson; Danna Jennings; John Seibyl; Alberto Ascherio Journal: Mov Disord Date: 2011-04-29 Impact factor: 10.338
Authors: Alberto Ascherio; Peter A LeWitt; Kui Xu; Shirley Eberly; Arthur Watts; Wayne R Matson; Connie Marras; Karl Kieburtz; Alice Rudolph; Mikhail B Bogdanov; Steven R Schwid; Marsha Tennis; Caroline M Tanner; M Flint Beal; Anthony E Lang; David Oakes; Stanley Fahn; Ira Shoulson; Michael A Schwarzschild Journal: Arch Neurol Date: 2009-12