4.5 Article

Serum uric acid level as a putative biomarker in Parkinson ? s disease patients carrying GBA1 mutations: 2-Year data from the PPMI study

Journal

PARKINSONISM & RELATED DISORDERS
Volume 84, Issue -, Pages 1-4

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.parkreldis.2020.12.020

Keywords

Uric acid; Biomarker; Glucocerebrosidase gene; Progression

Funding

  1. PPMI study, Parkinson's Progression Markers Initiative
  2. Michael J. Fox Foundation for Parkinson's Research
  3. Abbvie
  4. Avid
  5. Biogen
  6. Bristol-Myers Squibb
  7. Covance
  8. GE Healthcare
  9. Genentech
  10. GlaxoSmithKline
  11. Lilly
  12. Lundbeek
  13. Merck
  14. Meso Scale Discovery
  15. Pfizer
  16. Piramal
  17. Roche
  18. Servier
  19. Teva
  20. UCB
  21. Golub Capital

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The study evaluated serum uric acid levels in PD patients with mutations in the GBA1 gene and found that these patients had lower uric acid levels compared to healthy controls over a 2-year period. This suggests that low serum uric acid might serve as a progression biomarker in GBA-PD, but further studies are needed to confirm this association.
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.

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