Cited by 34Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchMedicinal Plants and Neuroprotection

Geniposide Attenuates the Phosphorylation of Tau Protein in Cellular and Insulin‐deficient APP/PS1 Transgenic Mouse Model of Alzheimer's Disease

Zhang, Yonglan, Yin, Fei, Liu, Jianhui, Liu, Zixuan·2016·Chemical Biology & Drug Design

Abstract

Our previous studies have shown that geniposide plays an essential role in glucose‐stimulated insulin secretion from pancreatic β cells and also regulates the metabolism of Aβ and its deposition in neurons. In this study, we reported that insulin deficiency induced significant increase of tau phosphorylation. Administration of geniposide for 4 weeks significantly decreased the phosphorylated level of tau and the acceleration of GSK‐3β phosphorylation in the brain of APP/PS1 transgenic mice induced by insulin deficiency. We also observed that geniposide decreased the phosphorylation of tau protein directly and increased the phosphorylation of Akt in primary cultured cortical neurons. Furthermore, geniposide enhanced the role of insulin on the phosphorylation of Akt, GSK‐3β, and tau in primary cultured cortical neurons. And these effects of geniposide in cortical neurons could be prevented by preincubation with LY294002, an inhibitor of PI3K. Taken together, our findings provide a mechanistic and perhaps a foundational link between diabetes and Alzheimer's disease and are consistent with the notion that geniposide might play an essential role on the phosphorylation of tau protein via enhancing insulin signaling and may convey a therapeutic benefit in Alzheimer's disease.

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Crossref · 10.1111/cbdd.12673

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  • High fat diet is thought to contribute directly to several key aspects of AD, including increased accumulation of Aβ, tau hyperphosphorylation, and inflammation of peripheral organs and brain.

    “High fat diet is thought to contribute directly to several key aspects of AD, including increased accumulation of Aβ, tau hyperphosphorylation, and inflammation of peripheral organs and brain [595–597].”

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Authors
Zhang, Y., Yin, F., Liu, J., & Liu, Z.
Affiliations
  • Chongqing University of Technology (CN)
  • Chongqing Technology and Business University (CN)
Corresponding author
Yin, Fei
Venue
Chemical Biology & Drug Design
Publisher
Wiley
Published
2015-11-12
Volume
87
Issue
3
Pages
409-418
ISSN
  • 1747-0277 (ISSN-L)
  • 1747-0285
OpenAlex
W2106039436
Cited by
34
References
43
Citations by year
2025: 3 · 2024: 5 · 2023: 3 · 2021: 4 · 2020: 2 · 2019: 5 · 2018: 6 · 2017: 4 · 2016: 2
FWCI
2.95
Type
journal article
Language
en
Open access
closed
Locations
  • Chemical Biology & Drug Design (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (81173063)
  • Chongqing Science and Technology Commission (2014jcyjjq10003, 2013jjb10032)
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
geniposide, tau phosphorylation, insulin deficiency, Alzheimer's disease, APP/PS1 mice, GSK3β, Akt phosphorylation, insulin signaling, phosphatidylinositol 3-kinase, cortical neurons, diabetes mellitus, neuroprotection
MeSH terms
Alzheimer Disease, Animals, Disease Models, Animal, Humans, Insulin, Mice, Transgenic, Phosphorylation, Amyloid beta-Protein Precursor, tau Proteins, Iridoids, Mice, Presenilin-1

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