Chlorogenic Acid Alleviates Aβ25-35-Induced Autophagy and Cognitive Impairment via the mTOR/TFEB Signaling Pathway
Open accessAbstract
Purpose: Chlorogenic acid (CGA), a phenolic acid isolated from fruits and vegetables, has been established to have neuroprotective properties in relation to Alzheimer’s disease (AD). However, the precise mechanism by which CGA prevents cognitive deficits in AD has not been well studied. This study aimed to explore the potential molecular mechanism of CGA action using an Aβ 25-35- induced SH-SY5Y neuron injury and cogxnitive deficits model in APP/PS1 mice. Methods: Three-month-old male APP/PS1 double transgenic mice and a human neuroblastoma cell line (SH-SY5Y) were used to assess the effects of CGA on AD in vivo and in vitro, respectively. Cognitive function in mice was measured using a Morris water maze (MWM) test. Hematoxylin and eosin, monodansylcadaverine fluorescence, LysoTracker Red (LTR), and immunofluorescence staining were used to evaluate the morphological changes in vivo and in vitro. The protein expressions of autophagy markers (LC3B-II/LC3B-I, p62/SQSTM, beclin1 and Atg5) and lysosomal-function-related markers (cathepsin D, mTOR, p-mTOR P70S6K, p-p70s6k and TFEB) were analyzed with Western blot analyses. Results: CGA treatment significantly improved spatial memory, relieved neuron damage, and inhibited autophagy in APP/PS1 mice (P< 0.05). Moreover, CGA notably suppressed autophagosome production and enhanced autophagy flux in SH-SY5Y cells induced by Aβ 25-35 (P< 0.05). Further analysis showed that CGA markedly promoted lysosomal activity, and this was accompanied by upregulated cathepsin D protein expression, which was induced by the mTOR/TFEB signaling pathway in APP/PS1 mice and Aβ 25-35 -exposed SH-SY5Y cells (P< 0.05). Conclusion: CGA treatment restored autophagic flux in the brain and alleviated cognitive impairments in APP/PS1 mice via enhanced activation of the mTOR/TFEB signaling pathway. Keywords: autophagy, chlorogenic acid, cognitive impairment, TFEB
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Chlorogenic acids treatment significantly inhibited autophagy caused by Aβ25-35 by modulating lysosomal function in SH-SY5Y cells, thereby attenuating loss of CA1 neurons and cognitive defects in APP/PS1 mice.
“Gao et al. [152] demonstrated that chlorogenic acids treatment significantly inhibited autophagy caused by Aβ25-35 by modulating lysosomal function in SH-SY5Y cells, thereby attenuating the loss of CA1 neurons and cognitive defects in APP/PS1 mice”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [152]
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References 46 · Cited by 115
- Authors
- Gao, L., Li, X., Meng, S., Ma, T., Wan, L., & Xu, S.
- Affiliations
- Chengdu University of Traditional Chinese Medicine (CN)
- Sichuan University (CN)
- Corresponding author
- Xu, Shijun
- Venue
- Drug Design Development and Therapy
- Publisher
- Informa UK Limited
- Published
- 2020-05
- Volume
- Volume 14
- Pages
- 1705-1716
- ISSN
- 1177-8881 (ISSN-L)
- PMC
- PMC7221680
- OpenAlex
- W3022797020
- Cited by
- 115
- References
- 46
- Citations by year
- 2026: 8 · 2025: 14 · 2024: 24 · 2023: 33 · 2022: 17 · 2021: 16 · 2020: 3
- FWCI
- 10.36
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Drug Design Development and Therapy (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
- Funders
- National Natural Science Foundation of China (81430100)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
- Keywords
- chlorogenic acid, Alzheimer's disease, amyloid beta 25-35, autophagy, cognitive impairment, APP/PS1 mice, SH-SY5Y cells, lysosomal activity, cathepsin D, autophagic flux, neuroprotection, spatial memory
- MeSH terms
- Administration, Oral, Alzheimer Disease, Animals, Autophagy, Cell Survival, Chlorogenic Acid, Dose-Response Relationship, Drug, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Peptide Fragments, Structure-Activity Relationship, Tumor Cells, Cultured, Molecular Structure, Signal Transduction, Amyloid beta-Peptides, Maze Learning, Mice, TOR Serine-Threonine Kinases, Cognitive Dysfunction, Optical Imaging
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