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Cited by 98Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchMedicinal Plants and Neuroprotection

Chenodeoxycholic Acid Ameliorates AlCl3-Induced Alzheimer’s Disease Neurotoxicity and Cognitive Deterioration via Enhanced Insulin Signaling in Rats

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Bazzari, Firas H., Abdallah, Dalaal M., El-Abhar, Hanan S.·2019·Molecules
DOI 10.3390/molecules24101992PMC PMC6571973
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Abstract

Insulin resistance is a major risk factor for Alzheimer’s disease (AD). Chenodeoxycholic acid (CDCA) and synthetic Farnesoid X receptor (FXR) ligands have shown promising outcomes in ameliorating insulin resistance associated with various medical conditions. This study aimed to investigate whether CDCA treatment has any potential in AD management through improving insulin signaling. Adult male Wistar rats were randomly allocated into three groups and treated for six consecutive weeks; control (vehicle), AD-model (AlCl3 50 mg/kg/day i.p) and CDCA-treated group (AlCl3 + CDCA 90 mg/kg/day p.o from day 15). CDCA improved cognition as assessed by Morris Water Maze and Y-maze tests and preserved normal histological features. Moreover, CDCA lowered hippocampal beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) and amyloid-beta 42 (Aβ42). Although no significant difference was observed in hippocampal insulin level, CDCA reduced insulin receptor substrate-1 phosphorylation at serine-307 (pSer307-IRS1), while increased protein kinase B (Akt) activation, glucose transporter type 4 (GLUT4), peroxisome proliferator-activated receptor gamma (PPARγ) and glucagon-like peptide-1 (GLP-1). Additionally, CDCA activated cAMP response element-binding protein (CREB) and enhanced brain-derived neurotrophic factor (BDNF). Ultimately, CDCA was able to improve insulin sensitivity in the hippocampi of AlCl3-treated rats, which highlights its potential in AD management.

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  • Chenodeoxycholic acid ameliorated the neurotoxic effect of Al by improving insulin sensitivity.

    “Chenodeoxycholic acid ameliorated the neurotoxic effect of Al by improving insulin sensitivity (Bazzari et al., 2019).”

    From Aluminium toxicosis: a review of toxic actions and effects (2019) · cites this paper as Bazzari et al., 2019

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Authors
Bazzari, F. H., Abdallah, D. M., & El-Abhar, H. S.
Affiliations
Cairo University (EG)
Corresponding author
Bazzari, Firas H.
ORCID
Venue
Molecules
Publisher
MDPI AG
Published
2019-05-24
Volume
24
Issue
10
Pages
1992
ISSN
1420-3049 (ISSN-L)
DOI
10.3390/molecules24101992
PMC
PMC6571973
OpenAlex
W2945348958
Cited by
98
References
7
Citations by year
2026: 9 · 2025: 10 · 2024: 19 · 2023: 15 · 2022: 22 · 2021: 12 · 2020: 8 · 2019: 2 · 2018: 1
FWCI
7.55
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecules (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Cairo University
  • Faculty of Pharmacy, Cairo University
  • Faculty of Veterinary Medicine, Cairo University
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
Keywords
chenodeoxycholic acid, Alzheimer's disease, aluminum chloride-induced neurotoxicity, insulin resistance, insulin signaling, IRS-1, Akt, PPARγ, glucagon-like peptide-1, CREB, brain-derived neurotrophic factor, BACE1, amyloid-beta 42, hippocampus, cognitive impairment, farnesoid X receptor
MeSH terms
Aluminum Chloride, Alzheimer Disease, Animals, Chenodeoxycholic Acid, Disease Models, Animal, Hippocampus, Insulin, Male, Models, Biological, Nerve Degeneration, Signal Transduction, Amyloid beta-Peptides, Rats, Wistar, Cyclic AMP Response Element-Binding Protein, Brain-Derived Neurotrophic Factor, Neurotoxicity Syndromes, PPAR gamma, Glucagon-Like Peptide 1, Cognitive Dysfunction, Spatial Memory

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