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136 Mitochondrial biomarkers in parkinson’s disease
  1. Ryan L Davis1,
  2. Siew L Wong2,
  3. Phillipa J Carling2,
  4. Thomas Payne2,
  5. Carolyn M Sue1,3,
  6. Oliver Bandmann2
  1. 1Department of Neurogenetics, University of Sydney, Australia
  2. 2Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield
  3. 3Department of Neurology, Royal North Shore Hospital, Sydney, Australia


Background There is strong evidence of mitochondrial dysfunction in both familial and sporadic Parkinson’s disease (PD). A biomarker reliably identifying mitochondrial dysfunction would be particularly important for future stratified/personalized medicine trials in Parkinson’s disease. A previous comparison of serum biomarkers in mitochondrial disease established that serum growth differentiation factor 15 (GDF-15) outperforms fibroblast growth factor-21 (FGF-21) and distinguishes patients with mitochondrial diseases from those without them.

Objective To systematically assess GDF-15, FGF-21 and mitochondrial DNA copy number (mtDNA) levels in the serum of patients with sporadic PD and controls to determine their utility as a suitable mitochondrial biomarker panel for PD.

Methods 120 patients with PD and 102 age-matched controls were recruited from a single centre. GDF-15, FGF-21 and mtDNA copy number were quantified using previously established assays.

Results FGF-21 concentrations did not significantly differ between groups. GDF-15 serum levels were significantly raised in late onset PD compared to controls and early onset PD. There was no difference in mtDNA between groups. None of the biomarkers tested showed a significant association with disease following multivariate logistic regression analysis.

Conclusion Serum FGF-21, GDF-15 and blood mtDNA could not accurately differentiate between PD and controls when assessed as candidate biomarkers.

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