Cited by 52Alzheimer's disease research and treatmentsCurcumin's Biomedical ApplicationsNeuroinflammation and Neurodegeneration Mechanisms

Curcumin Reduces Cognitive Deficits by Inhibiting Neuroinflammation through the Endoplasmic Reticulum Stress Pathway in Apolipoprotein E4 Transgenic Mice

Open access
Kou, Jiejian, Wang, Minghui, Shi, Junzhuo, Zhang, Haiyu, Pu, Xiaohui, Song, Shiyong, Yang, Cuiling, Yan, Yi +3 more·2021·ACS Omega

Abstract

Apolipoprotein E4 (ApoE4) is the main genetic risk factor for Alzheimer's disease (AD), but the exact way in which it causes AD remains unclear. Curcumin is considered to have good therapeutic potential for AD, but its mechanism has not been clarified. This study aims to observe the effect of curcumin on ApoE4 transgenic mice and explore its possible molecular mechanism. Eight-month-old ApoE4 transgenic mice were intraperitoneally injected with curcumin for 3 weeks, and the Morris water maze test was used to evaluate the cognitive ability of the mice. Immunofluorescence staining, immunohistochemistry, western blotting, and enzyme-linked immunosorbent assay (ELISA) were used to examine the brain tissues of the mice. Curcumin reduced the high expression of ApoE4 and the excessive release of inflammatory factors in ApoE4 mice. In particular, the expression of marker proteins of endoplasmic reticulum (ER) stress was significantly increased in ApoE4 mice, while curcumin significantly reduced the increase in the expression of these proteins. Collectively, curcumin alleviates neuroinflammation in the brains of ApoE4 mice by inhibiting ER stress, thus improving the learning and cognitive ability of transgenic mice.

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  • Curcumin's ability to decrease amyloid-beta plaques, as well as its antioxidant and anti-inflammatory properties, potentially explains enhanced cognitive function in curcumin-treated animal models.

    “Furthermore, various studies using animal models of AD have demonstrated enhanced cognitive function in curcumin-treated groups, potentially due to curcumin’s ability to decrease the levels of Aβ plaques, as well as its antioxidant and anti-inflammatory properties [154,155].”
  • Various studies using animal models of Alzheimer's disease demonstrate enhanced cognitive function in curcumin-treated groups.

    “Furthermore, various studies using animal models of AD have demonstrated enhanced cognitive function in curcumin-treated groups, potentially due to curcumin’s ability to decrease the levels of Aβ plaques, as well as its antioxidant and anti-inflammatory properties [154,155].”

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Authors
Kou, J., Wang, M., Shi, J., Zhang, H., Pu, X., Song, S., Yang, C., Yan, Y., Döring, Y., Xie, X., & Pang, X.
Affiliations
  • School of Pharmacy, Henan University, North Section of Jinming Avenue, Kaifeng 475004, Henan, China
  • Henan University (CN)
  • German Centre for Cardiovascular Research (DE)
  • University of Bern (CH)
Corresponding author
  • Xie, Xinmei
  • Pang, Xiaobin
Venue
ACS Omega
Published
2021-03-02
Volume
6
Issue
10
Pages
6654-6662
ISSN
2470-1343 (ISSN-L)
OpenAlex
W3134771782
Cited by
52
References
55
Citations by year
2026: 7 · 2025: 12 · 2024: 8 · 2023: 12 · 2022: 11 · 2021: 2
FWCI
5.18
Type
journal article
Language
en
Open access
Locations
  • ACS Omega (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Bern Open Repository and Information System (University of Bern) (submittedVersion, cc-by-nc-nd)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Open Access CRIS of the University of Bern
Funders
  • National Natural Science Foundation of China (31872311)
  • Henan Province (212300410027)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Curcumin's Biomedical Applications
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
curcumin, APOE ε4, Alzheimer's disease, neuroinflammation, endoplasmic reticulum stress, cognitive impairment, neuroprotection, learning and memory

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