ArticleBrain communications2021
Impaired dopamine metabolism is linked to fatigability in mice and fatigue in Parkinson's disease patients.
Article in Brain communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Functional, radiological and survival outcomes in rheumatoid arthritis-associated interstitial lung disease: 24-month results from the BERTHA prospective cohort.BMJ open respiratory research · 2026Article
- The role of L-DOPA in neurological and neurodegenerative complications: a review.Molecular and cellular biochemistry · 2025Review
- Resolution of Lipopolysaccharide-Induced Inflammation Followed by DNA Hypomethylation and Increased Tetrahydrobiopterin Biosynthesis in Mouse Hippocampus.Brain sciences · 2025Article
- Interpretable Machine Learning for Cross-Cohort Prediction of Motor Fluctuations in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Pain Hypersensitivity and Increased Urinary Tetrahydrobiopterin Levels in Mice Submitted to High-Fat Diet.Brain sciences · 2025Article
- Caffeine plus haloperidol reduces fatigue in an experimental model of Parkinson's disease - a prospective to APurinergic signalling · 2024Article
- Adenosine AFrontiers in pharmacology · 2024Article
- Dietary Polysaccharides Exert Anti-Fatigue Functions via the Gut-Muscle Axis: Advances and Prospectives.Foods (Basel, Switzerland) · 2023Review
- Crucial neuroprotective roles of the metabolite BH4 in dopaminergic neurons.bioRxiv : the preprint server for biology · 2023Article
- Tetrahydrobiopterin: Beyond Its Traditional Role as a Cofactor.Antioxidants (Basel, Switzerland) · 2023Review
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Fatigue is a common symptom of Parkinson's disease that compromises significantly the patients' quality of life. Despite that, fatigue has been under-recognized as symptom, its pathophysiology remains poorly understood, and there is no adequate treatment so far. Parkinson's disease is characterized by the progressive loss of midbrain dopaminergic neurons, eliciting the classical motor symptoms including slowing of movements, muscular rigidity and resting tremor. The dopamine synthesis is mediated by the rate-limiting enzyme tyrosine hydroxylase, which requires tetrahydrobiopterin as a mandatory cofactor. Here, we showed that reserpine administration (1 mg/kg, two intraperitoneal injections with an interval of 48 h) in adult Swiss male mice (8-10 weeks; 35-45 g) provoked striatal depletion of dopamine and tetrahydrobiopterin, and intolerance to exercise. The poor exercise performance of reserpinized mice was not influenced by emotional or anhedonic factors, mechanical nociceptive thresholds, electrocardiogram pattern alterations or muscle-impaired bioenergetics. The administration of levodopa (100 mg/kg; i.p.) plus benserazide (50 mg/kg; i.p.) rescued reserpine-induced fatigability-like symptoms and restored striatal dopamine and tetrahydrobiopterin levels. Remarkably, it was observed, for the first time, that impaired blood dopamine metabolism inversely and idependently correlated with fatigue scores in eighteen idiopathic Parkinson's disease patients (male
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