Abstract
Bile acids are commonly known as digestive agents for lipids. The mechanisms of bile acids in the gastrointestinal track during normal physiological conditions as well as hepatic and cholestatic diseases have been well studied. Bile acids additionally serve as ligands for signaling molecules such as nuclear receptor Farnesoid X receptor and membrane-bound receptors, Takeda G-protein-coupled bile acid receptor and sphingosine-1-phosphate receptor 2. Recent studies have shown that bile acid signaling may also have a prevalent role in the central nervous system. Some bile acids, such as tauroursodeoxycholic acid and ursodeoxycholic acid, have shown neuroprotective potential in experimental animal models and clinical studies of many neurological conditions. Alterations in bile acid metabolism have been discovered as potential biomarkers for prognosis tools as well as the expression of various bile acid receptors in multiple neurological ailments. This review explores the findings of recent studies highlighting bile acid-mediated therapies and bile acid-mediated signaling and the roles they play in neurodegenerative and neurological diseases.
Highlights
Bile acids are amphipathic molecules synthesized in the liver, stored in the gallbladder and released into the intestinal lumen in response to food intake as a digestion mechanism
We focused on the signaling pathways of bile acids relevant to the CNS and their direct influence in the pathologies of neurological and neurodegenerative diseases
These midpoint metabolites are transported from peripheral tissues back to the liver to be converted to primary bile acids cholic acid (CA) and chenodeoxycholic acid (CDCA) [11]
Summary
Bile acids are amphipathic molecules synthesized in the liver, stored in the gallbladder and released into the intestinal lumen in response to food intake as a digestion mechanism Their primary function is to serve as detergents in the solubilization of dietary lipids and fat-soluble vitamins. The alternative pathway catabolizes cholesterol in all tissues; cholesterol is metabolized via mitochondrial CYP27A1, converting it into 27-hydroxycholesterol For further conversion, these midpoint metabolites are transported from peripheral tissues back to the liver to be converted to primary bile acids CA and CDCA [11]. Located on the membranes of ileocytes, proximal renal tubule cells and cholangiocytes, ASBT facilitates the absorption of the majority of bile acids lacking passive diffusion qualifications or reclaims bile acids in systemic circulation for portal venous distribution back to the liver, minimizing excretion in urine. UGT has been identified in several neural cell types: neurons [30], astrocytes [30,31] and microglia [32]
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