Uric Acid Dynamics in Parkinson's Disease
Summary
Uric acid, the end product of purine metabolism in humans, has emerged as a key modulator of Parkinson’s disease (PD) through its antioxidant properties. Epidemiological studies consistently report lower serum uric acid levels in patients with PD compared to healthy controls, with further declines as the disease advances. This inverse relationship has prompted investigations into uric acid as both a biomarker for disease risk and progression and a potential neuroprotective agent. Mechanistically, uric acid scavenges reactive oxygen species, mitigates oxidative stress in dopaminergic neurons of the substantia nigra and influences intracellular redox balance. Fluctuations in uric acid levels may also reflect dysregulation of urate transporters and altered purine metabolism in the central nervous system. Beyond observational associations, experimental models demonstrate that augmenting intracellular urate preserves neuronal viability under toxin‐induced stress and modulates neuroinflammatory pathways. Clinically, dynamic measures of uric acid correlate with motor phenotype, non-motor symptoms and cognitive decline, underscoring its prognostic value. Emerging work integrates uric acid metrics with neuroimaging and machine-learning approaches to predict therapeutic responsiveness, notably to subthalamic nucleus deep brain stimulation. Together, these findings position uric acid dynamics at the interface of pathophysiological insight and personalised management in PD, with implications for global research and clinical strategies.
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Uric Acid Dynamics in Parkinson's Disease publication trend
The graph below shows the total number of articles in uric acid dynamics in parkinson's disease across all publications each year (not limited to Nature Index journals).
Technical terms
Uric acid: A natural antioxidant and final product of purine metabolism that scavenges reactive oxygen species and may protect dopaminergic neurons.
Oxidative stress: An imbalance between free radicals (reactive oxygen species) and antioxidant defences leading to cellular damage.
Resting-state functional MRI (rs-fMRI): A neuroimaging technique that measures spontaneous brain activity and connectivity when the subject is not performing a task.
Subthalamic nucleus deep brain stimulation (STN-DBS): A neurosurgical intervention in PD that delivers electrical impulses to the subthalamic nucleus to alleviate motor symptoms.
Xanthine oxidase: An enzyme that catalyses oxidation of hypoxanthine and xanthine to uric acid, generating reactive oxygen species as by-products.
References
- Prediction of STN-DBS for Parkinson’s disease by uric acid-related brain function connectivity: A machine learning study based on resting state function MRI. Frontiers in Aging Neuroscience (2023).
- Elevated Serum Xanthine Oxidase and Its Correlation with Antioxidant Status in Patients with Parkinson’s Disease. Biomolecules (2024).
- Serum uric acid levels in patients with Parkinson’s disease: A meta-analysis. PLOS ONE (2017).
- Nrf2 Signaling Contributes to the Neuroprotective Effects of Urate against 6-OHDA Toxicity. PLOS ONE (2014).
- Urate and Its Transgenic Depletion Modulate Neuronal Vulnerability in a Cellular Model of Parkinson's Disease. PLOS ONE (2012).
- Urate inhibits microglia activation to protect neurons in an LPS-induced model of Parkinson’s disease. Journal of Neuroinflammation (2018).
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