Bile acid signaling in neurodegenerative and neurological disorders
Open accessAbstract
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.
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Changes in the GM's composition correspond to changes in blood and brain BA profiles, and specific BA ligands' physicochemical properties determine the potency of BA receptor activation.
“Changes in the GM’s composition correspond to changes in blood and brain BA profiles, which are essential because specific BA ligands’ distinct physicochemical properties determine the potency of BA receptor activation (320–323).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [320]
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- [17]Chen I. Cassaro S. Physiology, Bile Acids StatPearls Treasure Island, FL, USA 2020 31747172
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Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis
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Bile acids as key modulators of the brain-Gut-Microbiota axis in alzheimer’s disease
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[Retracted] A Review of Bile Acid Metabolism and Signaling in Cognitive Dysfunction‐Related Diseases
Weng, Z.-B., Chen, Y.-R., Lv, J.-T., Wang, M.-X., Chen, Z.-Y., Zhou, W., Shen, X.-C., Zhan, L.-B., & Wang, F. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/4289383 · Cited by 32 · see citing works
Retracted
- Authors
- Grant, S. M., & DeMorrow, S.
- Affiliations
- The University of Texas at Austin (US)
- Central Texas Veterans Health Care System (US)
- Corresponding author
- DeMorrow, Sharon
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2020-08-20
- Volume
- 21
- Issue
- 17
- Pages
- 5982
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC7503576
- OpenAlex
- W3053917570
- Cited by
- 185
- References
- 138
- Citations by year
- 2026: 34 · 2025: 37 · 2024: 31 · 2023: 23 · 2022: 35 · 2021: 24 · 2020: 1
- FWCI
- 2.23
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK082435, DK112803)
- U.S. Department of Veterans Affairs (BX002638)
- Topics
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Aldose Reductase and Taurine
- Keywords
- bile acids, bile acid signaling, neurodegenerative diseases, neurological disorders, farnesoid X receptor, TGR5, S1PR2, tauroursodeoxycholic acid, ursodeoxycholic acid, neuroprotection, bile acid metabolism, biomarkers, bile acid receptors
- MeSH terms
- Receptor, Farnesoid X-Activated, Animals, Bile Acids and Salts, Brain, Humans, Liver, Nervous System Diseases, Retinal Diseases, Signal Transduction, Receptors, Cytoplasmic and Nuclear, Neurodegenerative Diseases, Receptors, G-Protein-Coupled
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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