ArticleMolecular neurobiology2018
Tauroursodeoxycholic Acid Improves Motor Symptoms in a Mouse Model of Parkinson's Disease.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 93 citations in OpenAlex.
- A Double-Blind, Randomized, Placebo-Controlled Trial of Ursodeoxycholic Acid (UDCA) in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2023Trial
- Review
- Dynamic alterations and potential roles of gut microbiota and metabolites in Angiostrongylus cantonensis-infected mice and rats.Infectious diseases of poverty · 2026Article
- The role of gut microbiota-mitochondria crosstalk in neurodegeneration: Underlying mechanisms and potential therapies.Neural regeneration research · 2026Article
- Reduced cerebrospinal fluid taurine is associated with nigrostriatal dopaminergic deficits in drug-naïve Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Endothelial IRE1 signaling maintains blood-brain barrier integrity and limits neuroinflammation after traumatic brain injury.Cell death & disease · 2026Article
- Neuroprotection in Parkinson Disease.Neurology and therapy · 2025Review
- TUDCA combined with Syndopa protects the midbrain and gut from MPTP toxicity in a Parkinson's disease mouse model: Immunohistochemical evidence.Biomolecules & biomedicine · 2025Article
- The role of gut microbiota-derived metabolites in neuroinflammation.Neuroprotection (Chichester, England) · 2025Review
- Beyond weight loss: exploring the neurological ramifications of altered gut microbiota post-bariatric surgery.Journal of translational medicine · 2025Review
- The effects of ursodeoxycholic acid on Parkinson's disease, a mechanistic review of the recent evidence.Metabolic brain disease · 2025Review
- Gut microbiota: A new window for the prevention and treatment of neuropsychiatric disease.Journal of central nervous system disease · 2025Review
- Article
- Gut microbiota and healthy longevity.Science China. Life sciences · 2024Review
- Metabolomics Unveils Disrupted Pathways in Parkinson's Disease: Toward Biomarker-Based Diagnosis.ACS chemical neuroscience · 2024Article
- Emerging Roles of Bile Acids and TGR5 in the Central Nervous System: Molecular Functions and Therapeutic Implications.International journal of molecular sciences · 2024Review
- Diagnostic Potential of Alternations of Bile Acid Profiles in the Plasma of Patients with Huntington's Disease.Metabolites · 2024Article
- Identification of metabolites reproducibly associated with Parkinson's Disease via meta-analysis and computational modelling.NPJ Parkinson's disease · 2024Article
- Research progress on intranasal treatment for Parkinson's disease.Neuroprotection (Chichester, England) · 2024Review
- Identification of Bile Acid-Derived Chemical Chaperone(s) Targeting E46K-Mutated Alpha-Synuclein Protein to Treat Parkinson's Disease: Molecular Modelling, Docking, ADME, and Simulation Studies.Applied biochemistry and biotechnology · 2024Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Parkinson's disease (PD) is characterized by severe motor symptoms, and currently there is no treatment that retards disease progression or reverses damage prior to the time of clinical diagnosis. Tauroursodeoxycholic acid (TUDCA) is neuroprotective in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD; however, its effect in PD motor symptoms has never been addressed. In the present work, an extensive behavior analysis was performed to better characterize the MPTP model of PD and to evaluate the effects of TUDCA in the prevention/improvement of mice phenotype. MPTP induced significant alterations in general motor performance paradigms, including increased latency in the motor swimming, adhesive removal and pole tests, as well as altered gait, foot dragging, and tremors. TUDCA administration, either before or after MPTP, significantly reduced the swimming latency, improved gait quality, and decreased foot dragging. Importantly, TUDCA was also effective in the prevention of typical parkinsonian symptoms such as spontaneous activity, ability to initiate movement and tremors. Accordingly, TUDCA prevented MPTP-induced decrease of dopaminergic fibers and ATP levels, mitochondrial dysfunction and neuroinflammation. Overall, MPTP-injected mice presented motor symptoms that are aggravated throughout time, resembling human parkinsonism, whereas PD motor symptoms were absent or mild in TUDCA-treated animals, and no aggravation was observed in any parameter. The thorough demonstration of improvement of PD symptoms together with the demonstration of the pathways triggered by TUDCA supports a subsequent clinical trial in humans and future validation of the application of this bile acid in PD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.