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Article: Expert insights: The potential role of the gut microbiome-bile acid-brain axis in the development and progression of Alzheimer's disease and hepatic encephalopathy

TitleExpert insights: The potential role of the gut microbiome-bile acid-brain axis in the development and progression of Alzheimer's disease and hepatic encephalopathy
Authors
KeywordsAlzheimer's disease
bile acid
farnesoid X receptor
gut microbiome
hepatic encephalopathy
Issue Date2020
Citation
Medicinal Research Reviews, 2020, v. 40, n. 4, p. 1496-1507 How to Cite?
AbstractRecent epidemiological and molecular studies have linked the disruption of cholesterol homeostasis to increased risk for developing Alzheimer's disease (AD). Emerging evidence also suggests that brain cholesterol accumulation contributes to the progression of hepatic encephalopathy (HE) via bile acid (BA)-mediated effects on the farnesoid X receptor. In this perspective paper, we reviewed several recently published studies that suggested a role for the gut microbiota transformation of BAs as a factor in AD and HE development/progression. We hypothesize that in addition to cholesterol elimination pathways, alteration of the gut microbiota and subsequent changes in both the serum and brain BA profiles are mechanistically involved in the development of both AD and HE, and thus, are a potential target for the prevention and treatment of the two diseases. Our understanding of the microbiome-BAs-brain axis in central nervous system disease is still evolving, and critical questions regarding the emerging links among central, peripheral, and intestinal metabolic failures contributing to brain health and disease during aging have yet to be addressed.
Persistent Identifierhttp://hdl.handle.net/10722/342243
ISSN
2023 Impact Factor: 10.9
2023 SCImago Journal Rankings: 2.864
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJia, Wei-
dc.contributor.authorRajani, Cynthia-
dc.contributor.authorKaddurah-Daouk, Rima-
dc.contributor.authorLi, Houkai-
dc.date.accessioned2024-04-17T07:02:23Z-
dc.date.available2024-04-17T07:02:23Z-
dc.date.issued2020-
dc.identifier.citationMedicinal Research Reviews, 2020, v. 40, n. 4, p. 1496-1507-
dc.identifier.issn0198-6325-
dc.identifier.urihttp://hdl.handle.net/10722/342243-
dc.description.abstractRecent epidemiological and molecular studies have linked the disruption of cholesterol homeostasis to increased risk for developing Alzheimer's disease (AD). Emerging evidence also suggests that brain cholesterol accumulation contributes to the progression of hepatic encephalopathy (HE) via bile acid (BA)-mediated effects on the farnesoid X receptor. In this perspective paper, we reviewed several recently published studies that suggested a role for the gut microbiota transformation of BAs as a factor in AD and HE development/progression. We hypothesize that in addition to cholesterol elimination pathways, alteration of the gut microbiota and subsequent changes in both the serum and brain BA profiles are mechanistically involved in the development of both AD and HE, and thus, are a potential target for the prevention and treatment of the two diseases. Our understanding of the microbiome-BAs-brain axis in central nervous system disease is still evolving, and critical questions regarding the emerging links among central, peripheral, and intestinal metabolic failures contributing to brain health and disease during aging have yet to be addressed.-
dc.languageeng-
dc.relation.ispartofMedicinal Research Reviews-
dc.subjectAlzheimer's disease-
dc.subjectbile acid-
dc.subjectfarnesoid X receptor-
dc.subjectgut microbiome-
dc.subjecthepatic encephalopathy-
dc.titleExpert insights: The potential role of the gut microbiome-bile acid-brain axis in the development and progression of Alzheimer's disease and hepatic encephalopathy-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/med.21653-
dc.identifier.pmid31808182-
dc.identifier.scopuseid_2-s2.0-85076089711-
dc.identifier.volume40-
dc.identifier.issue4-
dc.identifier.spage1496-
dc.identifier.epage1507-
dc.identifier.eissn1098-1128-
dc.identifier.isiWOS:000500717100001-

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