ArticleNPJ Parkinson's disease2025
Urea cycle dysregulation drives metabolic stress and neurodegeneration in Parkinson's disease.
Article in NPJ Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- AMPK activation by Aldometanib from Bigujing improves metabolic and cognitive dysfunction in aging mice.Metabolic brain disease · 2026Article
- ODC1-associated astrocytic urea cycle dysregulation in age-related memory impairment.Biogerontology · 2026Article
- The Kidney-Brain Axis in Chronic Kidney Disease: Uremic Toxins, Cognitive Decline, Mechanistic Pathways, Biomarkers and Therapeutic Perspectives.Biomedicines · 2026Review
- Parkinson's Disease: From Metabolism to Genetics-A Comprehensive Review.Current issues in molecular biology · 2026Review
- Extracellular vesicle signatures from eye lavage as novel non-invasive biomarkers for hypoxic ischaemic insult-findings from a neonatal mouse model.Frontiers in medical technology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Parkinson's disease (PD), common neurodegenerative disorder, involves substantia nigra dopaminergic neuron loss and α-synuclein accumulation in Lewy bodies. While pathogenesis remains unclear, dysregulated urea metabolism may play a central role. This study detected elevated serum urea levels in PD patients with upregulated urea cycle enzymes. In MPTP-induced PD mice, urea accumulated in the substantia nigra and striatum, alongside increased activity of urea cycle enzymes (ODC1, ARG1, OTC) and urea transporter UT-B. Mechanistically, brain urea accumulation likely stems from imbalanced urea cycle activity and impaired UT-B-mediated clearance, with compensatory UT-B upregulation specifically in the substantia nigra. In vitro, MPTP-treated neuronal cells showed increased enzyme and UT-B expression, while high urea directly suppressed tyrosine hydroxylase (TH). Importantly, ODC1 knockdown reversed urea dysmetabolism, restored TH, and alleviated neuronal damage. These findings establish ODC1-mediated urea cycle dysregulation as a core metabolic feature of PD, proposing ODC1 or urea metabolism as novel therapeutic targets.
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Registered trials
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