Roles of bile acids signaling in neuromodulation under physiological and pathological conditions.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic pathways with no original human clinical data
PubMed 37308953 · doi:10.1186/s13578-023-01053-z
What was done
This narrative review summarizes literature on bile acid metabolism (liver synthesis and brain CYP46A1-mediated pathways), mechanisms of crossing the blood-brain barrier, and downstream central and peripheral signaling pathways (including FXR-FGF15/19 and TGR5-GLP-1). It also discusses the proposed neuroprotective actions of ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid (TUDCA) in neurological conditions.
What was found
The abstract reports no numerical data or quantitative outcomes. It describes mechanisms whereby circulating bile acids cross the blood-brain barrier via passive diffusion or transporters, act on membrane, nuclear, and neurotransmitter receptors, and notes that UDCA and TUDCA attenuate neuroinflammation, apoptosis, oxidative stress, and endoplasmic reticulum stress.
Why it matters
It outlines how gut- and liver-derived bile acid signaling reaches the central nervous system, highlighting hydrophilic bile acids as potential therapeutic candidates for neurological disorders.
Limits
The abstract provides no original empirical data, quantitative findings, or systematic search protocol. Stated protective mechanisms rely primarily on preclinical models with unclear direct translation to human clinical outcomes.
Cited by
- supports TUDCA crosses the blood-brain barrier.