ArticleBiomolecules & biomedicine2025
TUDCA combined with Syndopa protects the midbrain and gut from MPTP toxicity in a Parkinson's disease mouse model: Immunohistochemical evidence.
Article in Biomolecules & biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- The Gut-Brain Axis: A Critical Link between Type 2 Diabetes and Parkinson's disease.Probiotics and antimicrobial proteins · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuro-inflammation plays a significant role in the neurodegenerative processes associated with Parkinson's disease (PD). A hallmark of PD is the degeneration of dopaminergic neurons within the nigrostriatal pathway. The standard treatment for PD is Syndopa (a combination of levodopa and carbidopa). However, while Syndopa alleviates symptoms, it is also associated with numerous side effects in patients. Research has demonstrated the protective effects of Tauroursodeoxycholic acid (TUDCA) in mitigating the neuropathological consequences of PD in several preclinical studies. Nonetheless, further investigation is necessary to delineate the role of TUDCA in PD therapeutics. Although the efficacy of TUDCA monotherapy in PD has been explored, there is a lack of preclinical research examining the additive effects of TUDCA in conjunction with Syndopa therapy. In this study, we utilized an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of PD to evaluate the potential therapeutic benefits of TUDCA monotherapy and the combined effects of TUDCA and Syndopa therapy, compared to standard Syndopa treatment. We conducted immunohistochemical (IHC) assessments of α-synuclein expression in the gut and substantia nigra pars compacta (SNpc), as well as tyrosine hydroxylase and NF-kB expression in the striatum and SNpc regions, to investigate the efficacy of the test drugs. The immunohistochemical findings indicate that both TUDCA monotherapy and the combination therapy of TUDCA and Syndopa significantly reduced MPTP-induced alterations in the expression levels of α-synuclein, tyrosine hydroxylase, and NFκB in the striatum and SNpc regions. Additionally, the MPTP-induced changes in α-synuclein expression in the gut were notably reversed by these treatments. Collectively, these results suggest that incorporating TUDCA with Syndopa may represent a promising therapeutic strategy to address the pathophysiological challenges associated with PD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.