Tauroursodeoxycholic acid (TUDCA) is neuroprotective in a chronic mouse model of Parkinson’s disease
Abstract
Objective: Parkinson’s disease (PD) is a progressive motor disease of unknown etiology. Although neuroprotective ability of endogenous bile acid, tauroursodeoxycholic acid (TUDCA), shown in various diseases, including an acute model of PD,the potential therapeutic role of TUDCA in progressive models of PD that exhibit all aspects of PD has not been elucidated. In the present study, mice were assigned to one of four treatment groups: (1) Probenecid (PROB); (2) TUDCA, (3) MPTP + PROB (MPTPp); and (3) TUDCA + MPTPp. Methods: Markers for dopaminergic function, neuroinflammation, oxidative stress and autophagy were assessed using high performance liquid chromatography (HPLC), immunohistochemistry (IHC) and western blot (WB) methods. Locomotion was measured before and after treatments. Results: MPTPp decreased the expression of dopamine transporters (DAT) and tyrosine hydroxylase (TH), indicating dopaminergic damage, and induced microglial and astroglial activation as demonstrated by IHC analysis. MPTPp also decreased DA and its metabolites as demonstrated by HPLC analysis. Further, MPTPp-induced protein oxidation; increased LAMP-1 expression indicated autophagy and the promotion of alpha-synuclein (α-SYN) aggregation. Discussion: Pretreatment with TUDCA protected against dopaminergic neuronal damage, prevented the microglial and astroglial activation, as well as the DA and DOPAC reductions caused by MPTPp. TUDCA by itself did not produce any significant change, with data similar to the negative control group. Pretreatment with TUDCA prevented protein oxidation and autophagy, in addition to inhibiting α-SYN aggregation. Although TUDCA pretreatment did not significantly affect locomotion, only acute treatment effects were measured, indicating more extensive assessments may be necessary to reveal potential therapeutic effects on behavior. Together, these results suggest that autophagy may be involved in the progression of PD and that TUDCA may attenuate these effects. The efficacy of TUDCA as a novel therapy in patients with PD clearly warrants further study.
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UDCA and TUDCA have neuroprotective effects in counteracting mitochondrial dysfunction, oxidative stress, and neuroinflammation in Parkinson's disease mouse models.
“Multiple in vivo studies have demonstrated the neuroprotective effects of UDCA and TUDCA in counteracting mitochondrial dysfunction, oxidative stress, and neuroinflammation within PD mouse models.386–392”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [389]
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- Authors
- Cuevas, E., Burks, S., Raymick, J., Robinson, B., Gómez-Crisóstomo, N. P., Escudero-Lourdes, C., Lopez, A. G. G., Chigurupati, S., Hanig, J., Ferguson, S. A., & Sarkar, S.
- Affiliations
- National Center for Toxicological Research (US)
- Universidad Juárez Autónoma de Tabasco (MX)
- National Center for Toxicological Research, US FDA
- Escuela Nacional Preparatoria-UNAM, Mexico
- United States Food and Drug Administration (US)
- Corresponding author
- Sarkar, Sumit
- ORCID
- Venue
- Nutritional Neuroscience
- Publisher
- Informa UK Limited
- Published
- 2020-12-21
- Volume
- 25
- Issue
- 7
- Pages
- 1374-1391
- ISSN
- 1028-415X (ISSN-L)
- 1476-8305
- OpenAlex
- W3113827240
- Cited by
- 57
- References
- 56
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 10 · 2023: 11 · 2022: 8 · 2021: 5
- FWCI
- 2.60
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nutritional Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- tauroursodeoxycholic acid, Parkinson's disease, neuroprotection, MPTP-induced neurotoxicity, dopaminergic neurons, dopamine transporter, tyrosine hydroxylase, microglial activation, astroglial activation, neuroinflammation, oxidative stress, protein oxidation, autophagy, alpha-synuclein aggregation, probenecid, bile acids
- MeSH terms
- Animals, Disease Models, Animal, Dopamine, Humans, Mice, Inbred C57BL, Parkinson Disease, Taurochenodeoxycholic Acid, Neuroprotective Agents, Mice, Dopaminergic Neurons
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