ArticleFrontiers in aging neuroscience2023
Uric acid regulates α-synuclein transmission in Parkinsonian models.
Article in Frontiers in aging neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Uric acid alleviates the inflammatory response in LPS-induced BV2 cells and MPTP-induced PD mice by resisting ferroptosis through the Nrf2 signalling pathway.Redox report : communications in free radical research · 2026Article
- A novel oxidative-inflammatory biomarker for Parkinson's disease: clinical utility of the uric acid-to-albumin ratio.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Drug repurposing for disease-modifying effects in multiple system atrophy.Translational neurodegeneration · 2026Review
- A review of the evidence for a protective role of uric acid in Parkinson's disease.NPJ Parkinson's disease · 2025Review
- Xanthine Oxidoreductase: A Double-Edged Sword in Neurological Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Targeting uric acid: a promising intervention against oxidative stress and neuroinflammation in neurodegenerative diseases.Cell communication and signaling : CCS · 2025Review
- Uric Acid: A Biomarker and Pathogenic Factor of Affective Disorders and Neurodegenerative Diseases.Current pharmaceutical design · 2025Review
- Role and mechanism of molecular hydrogen in the treatment of Parkinson's diseases.Frontiers in neuroscience · 2025Review
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Authors and funding
8 authors.
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Abstract
Ample evidence demonstrates that α-synuclein (α-syn) has a critical role in the pathogenesis of Parkinson's disease (PD) with evidence indicating that its propagation from one area of the brain to others may be the primary mechanism for disease progression. Uric acid (UA), a natural antioxidant, has been proposed as a potential disease modifying candidate in PD. In the present study, we investigated whether UA treatment modulates cell-to-cell transmission of extracellular α-syn and protects dopaminergic neurons in the α-syn-enriched model. In a cellular model, UA treatment decreased internalized cytosolic α-syn levels and neuron-to-neuron transmission of α-syn in donor-acceptor cell models by modulating dynamin-mediated and clathrin-mediated endocytosis. Moreover, UA elevation in α-syn-inoculated mice inhibited propagation of extracellular α-syn which decreased expression of phosphorylated α-syn in the dopaminergic neurons of the substantia nigra leading to their increased survival. UA treatment did not lead to change in markers related with autophagolysosomal and microglial activity under the same experimental conditions. These findings suggest UA may control the pathological conditions of PD via additive mechanisms which modulate the propagation of α-syn.
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