The effects of ursodeoxycholic acid on Parkinson's disease, a mechanistic review of the recent evidence.
Level 5 - mechanism / opinion, no new human data
Narrative mechanistic review of preclinical and clinical literature
PubMed 39891787 · doi:10.1007/s11011-025-01542-9
What was done
The authors conducted a literature review of in vitro, in vivo, and clinical studies retrieved from PubMed, Google Scholar, Scopus, Web of Science, and the Cochrane Library evaluating the effects and biological mechanisms of ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid (TUDCA) in Parkinson's disease.
What was found
The abstract reports no quantitative values, effect sizes, or study counts. It qualitatively summarizes three primary neuroprotective mechanisms of blood-brain barrier-permeable UDCA and TUDCA: anti-inflammatory action (lowering tumor necrosis factor-α and interleukin-1β), antioxidant defense (upregulating superoxide dismutase and glutathione peroxidase), and anti-apoptotic activity (reducing caspase-3 activation and striatal Bax expression).
Why it matters
Highlights the mechanistic rationale for repurposing endogenous bile acids like UDCA and TUDCA as potential mitochondrial-protective and disease-modifying agents in Parkinson's disease.
Limits
The abstract does not report the number of studies reviewed, systematic screening criteria, or quantitative results. Evidence is heavily based on preclinical models, and clinical efficacy in human Parkinson's disease remains unproven in this summary.
Cited by
- supports TUDCA crosses the blood-brain barrier.