ArticleJournal of inflammation research2025
Exploring Potential Causal Links: How Parkinson's Disease Brain Damage Impacts Liver Health-A Mendelian Randomization and Transcriptomic Study.
Article in Journal of inflammation research, 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
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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
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Who cites it
1 citing paper in PubMed.
- Beyond Organ Boundaries: Molecular Mechanisms of Hepatic Encephalopathy and Parkinson's Disease from the Perspective of the Gut-Liver-Brain Axis.Research (Washington, D.C.) · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by slow movements, muscle rigidity, tremors, and changes in gait and posture. Clinical studies have demonstrated a close association between PD and liver disease, but most research has focused on the impact of liver disorders on brain damage in PD, and further exploration is needed to understand the pathways and mechanisms underlying liver damage in patients with PD. Methods: This study employs Mendelian Randomization (MR) and transcriptomic analysis to investigate the causal impact of PD-related brain damage on liver health, identifying serum metabolites (eg, cysteine) and shared immune-inflammatory pathways as mediators. Results: The study indicates that PD-related brain damage does indeed have an impact on liver metabolic function. PD-related brain damage may disrupt the concentration of cysteine, which, when elevated, can cause liver cell damage and oxidative stress. Additionally, PD-related brain damage may affect specific genes (such as NCF1, NCF, and SELPLG) involved in immune and inflammatory responses that lead to liver damage. Interestingly, the anti-PD drug, tolcapone, has notable therapeutic effects but also negatively affects specific genes, contributing to liver damage in patients with PD. Conclusion: This study reveals the mechanisms by which PD affects liver metabolism and proposes cysteine as a biomarker and therapeutic target for liver damage in PD. Furthermore, the impact of PD treatment drugs on liver function was also evaluated. These findings provide important insights for the development of future PD treatment strategies, and further clinical research is needed to validate and optimize clinical interventions to maximize treatment efficacy and minimize side effects in patients with PD.
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