Serum uric acid level as a putative biomarker in Parkinson's disease patients carrying GBA1 mutations: 2-Year data from the PPMI study. (March 2021)

• Record Type: Journal Article
• Authors: Koros, Christos; Simitsi, Athina-Maria; Papagiannakis, Nikolaos; Bougea, Anastasia; Prentakis, Andreas; Papadimitriou, Dimitra; Pachi, Ioanna; Antonelou, Roubina; Angelopoulou, Efthalia; Beratis, Ion; Bozi, Maria; Papageorgiou, Sokratis G.; Trapali, Xenia Geronicola; Stamelou, Maria; Stefanis, Leonidas
• Is Part Of: Parkinsonism & related disorders. Volume 84(2021)
• Page Start: 1
• Page End: 4
• Publication Date: 2021-03
• Subjects: Parkinson's disease -- Uric acid -- Biomarker -- Glucocerebrosidase gene -- Progression; Parkinson's disease -- Periodicals; Movement disorders -- Periodicals; Movement Disorders -- Periodicals; Nerve Degeneration -- Periodicals; Nervous System Diseases -- Periodicals; Parkinson Disease -- Periodicals; Tremor -- Periodicals; Parkinson, Maladie de -- Périodiques; Parkinson's disease; 616.833
• DOI: 10.1016/j.parkreldis.2020.12.020
• Languages: English
• ISSNs: 1353-8020

Abstract

Abstract: Introduction: Blood uric acid represents an important biomarker in sporadic Parkinson's disease (PD). Whether uric acid levels change in genetic forms of PD is beginning to be assessed. The aim of the present study was to evaluate differences in serum uric acid level among PD patients harboring mutations in the glucocerebrosidase (GBA1) gene, sporadic PD, and healthy controls followed longitudinally. Methods: Longitudinal 2-year serum uric acid measurement data of 120 GBA-PD patients have been downloaded from the Parkinson's Progression Markers Initiative (PPMI) database. This cohort was compared with 369 de novo sporadic PD patients and 195 healthy controls enrolled in the same study. Results: Following adjustment for age, sex and BMI the GBA-PD cohort exhibited lower 2-year longitudinal uric acid level as compared to the controls (p = 0.016). Baseline uric acid measurements showed only a marginal difference (p = 0.119), but year 2 uric acid levels were lower in the GBA-PD cohort (p < 0.001). There was no difference in baseline, year 2 and 2-year longitudinal serum uric acid in the GBA-PD cohort as compared to sporadic PD (p = 0.664, p = 0.117 and p = 0.315). Conclusions: This is the first study to assess serum uric acid in a GBA-PD cohort. Our findings suggest that low serum uric acid might be a progression biomarker in GBA-PD. However, more studies (ideally longitudinal) on the association between low serum uric acid and clinical data in GBA-PD are needed. These results are consistent with data from previous reports assessing uric acid as a biomarker in other genetic forms of PD. Highlights: Serum uric acid levels were lower in PD patients carrying GBA1 mutations as compared to healthy controls. Serum uric acid did not differ between GBA-PD vs sporadic PD. There was a gradual decrease of uric acid levels in both PD cohorts.