Tauroursodeoxycholic acid (TUDCA) supplementation prevents cognitive impairment and amyloid deposition in APP/PS1 mice
Open accessAbstract
Alzheimer's disease (AD) is a neurodegenerative disease hallmarked by extracellular Aβ(1-42) containing plaques, and intracellular neurofibrillary tangles (NFT) containing hyperphosphorylated tau protein. Progressively, memory deficits and cognitive disabilities start to occur as these hallmarks affect hippocampus and frontal cortex, regions highly involved in memory. Connective tissue growth factor (CTGF) expression, which is high in the vicinity of Aβ plaques and NFTs, was found to influence γ-secretase activity, the molecular crux in Aβ(1-42) production. Tauroursodeoxycholic acid (TUDCA) is an endogenous bile acid that downregulates CTGF expression in hepatocytes and has been shown to possess therapeutic efficacy in neurodegenerative models. To investigate the possible in vivo therapeutic effects of TUDCA, we provided 0.4% TUDCA-supplemented food to APP/PS1 mice, a well-established AD mouse model. Six months of TUDCA supplementation prevented the spatial, recognition and contextual memory defects observed in APP/PS1 mice at 8 months of age. Furthermore, TUDCA-supplemented APP/PS1 mice displayed reduced hippocampal and prefrontal amyloid deposition. These effects of TUDCA supplementation suggest a novel mechanistic route for Alzheimer therapeutics.
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TUDCA treatment inhibits Aβ deposition and glial activation in APP/PS1 mice and HFD-fed A7-Tg mice.
“Notably, TUDCA treatment has demonstrated the ability to inhibit Aβ deposition and glial activation in APP/PS1 mice and HFD-fed A7-Tg mice.372–375”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [373]
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- Authors
- Lo, A. C., Callaerts-Vegh, Z., Nunes, A. F., Rodrigues, C. M. P., & D'Hooge, R.
- Affiliations
- KU Leuven (BE)
- University of Lisbon (PT)
- Corresponding author
- Rodrigues, Cecília M.P.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2013-02
- Volume
- 50
- Pages
- 21-29
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2023956551
- Cited by
- 120
- References
- 61
- Citations by year
- 2026: 9 · 2025: 9 · 2024: 15 · 2023: 12 · 2022: 9 · 2021: 14 · 2020: 9 · 2019: 8 · 2018: 7 · 2017: 5 · 2016: 4 · 2015: 6 · 2014: 10 · 2013: 3
- FWCI
- 4.07
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- 7FP grant MEMOSAD
- Federal Science Fund FWO-Vlaanderen (G.0327.08)
- Fundacão para a Ciência e a Tecnologia (PTDC/SAU-NMC/117877/2010)
- 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
- tauroursodeoxycholic acid, Alzheimer's disease, APP/PS1 mice, amyloid plaques, amyloid deposition, cognitive impairment, memory impairment, connective tissue growth factor, gamma-secretase, tau hyperphosphorylation, neurofibrillary tangles, hippocampus, prefrontal cortex, dietary supplementation, bile acids
- MeSH terms
- Alzheimer Disease, Animals, Behavior, Animal, Cholagogues and Choleretics, Cognition Disorders, Disease Models, Animal, Male, Mice, Transgenic, Taurochenodeoxycholic Acid, Amyloid beta-Protein Precursor, Dietary Supplements, Mice, Presenilin-1, Amyloidogenic Proteins
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