A Review published in Cell & Bioscience summarizes recent findings on the crosstalk of bile acids between brain and periphery and neurological functions of bile acids under both physiological and pathological conditions.
]. For example, TUDCA and UDCA substantially reduced PrP conversion in chronically and acutely infected cell cultures and decreased neuronal loss in prion-infected cerebellar slice cultures. Low dose UDCA treatment in early stage could prolong incubation periods, reduce astrocytosis and increase survival time in prion-infected male mice but not in female mice [].
]. Currently, the overall misfolded protein-diminishing or ER stress-alleviating activity of UDCA/TUDCA is still unclear and lack of enough substantial evidences in prion diseases and other neuropathological conditions.This review summarizes recent findings to highlight the crosstalk of BA between brain and periphery, and neurological functions of BA under both physiological and pathological conditions.
BA act as etiological factors or mediators linking the pathogenesis of various neurological diseases, supporting BA metabolites as potential risk biomarkers for prognosis of diseases. Due to the complex of BA metabolites in compositions and biochemical properties, how to figure out the exact function of specific BA metabolite or the overall contribution of altered BA profiles to the pathogenesis of neurological diseases remains to be solved in the future.
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Roles of bile acids signaling in neuromodulation under physiological and pathological conditions - Cell & BioscienceBile acids (BA) are important physiological molecules not only mediating nutrients absorption and metabolism in peripheral tissues, but exerting neuromodulation effect in the central nerve system (CNS). The catabolism of cholesterol to BA occurs predominantly in the liver by the classical and alternative pathways, or in the brain initiated by the neuronal-specific enzyme CYP46A1 mediated pathway. Circulating BA could cross the blood brain barrier (BBB) and reach the CNS through passive diffusion or BA transporters. Brain BA might trigger direct signal through activating membrane and nucleus receptors or affecting activation of neurotransmitter receptors. Peripheral BA may also provide the indirect signal to the CNS via farnesoid X receptor (FXR) dependent fibroblast growth factor 15/19 (FGF15/19) pathway or takeda G protein coupled receptor 5 (TGR5) dependent glucagon-like peptide-1 (GLP-1) pathway. Under pathological conditions, alterations in BA metabolites have been discovered as potential pathogenic contributors in multiple neurological disorders. Attractively, hydrophilic ursodeoxycholic acid (UDCA), especially tauroursodeoxycholic acid (TUDCA) can exert neuroprotective roles by attenuating neuroinflammation, apoptosis, oxidative or endoplasmic reticulum stress, which provides promising therapeutic effects for treatment of neurological diseases. This review summarizes recent findings highlighting the metabolism, crosstalk between brain and periphery, and neurological functions of BA to elucidate the important role of BA signaling in the brain under both physiological and pathological conditions.
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