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Cited by 301Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchAldose Reductase and Taurine

Diabetes mellitus and Alzheimer's disease: GSK-3β as a potential link

Zhang, Ying, Huang, Nan-qu, Yan, Fei, Jin, Hai, Zhou, Shao-yu, Shi, Jing-shan, Jin, Feng·2018·Behavioural Brain Research
DOI 10.1016/j.bbr.2017.11.015
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Abstract

It is well known that Alzheimer's disease (AD) is closely related to diabetes mellitus (DM), and AD is also regarded as Type 3 diabetes (T3D). However, the exact link between AD and DM is still unclear. Recently, more and more evidence has shown that glycogen synthase kinase-3β (GSK-3β) may be the potential link between DM and AD. In DM, GSK-3β is the crucial enzyme of glycogen synthesis, which plays a key role in regulating blood glucose. More importantly, GSK-3β is one of the key factors leading to insulin deficiency and insulin resistance, and insulin resistance is an important hallmark of the occurrence and development of DM. In AD, GSK-3β plays an important role in hyperphosphorylation of microtubule-associated protein tau (tau), which is one of the pathological features in AD. GSK-3β is one of the important kinases of tau phosphorylation and is involved in the insulin/phosphoinositide 3-kinase/protein kinase B (insulin/PI3K/Akt) signaling pathway. Dysfunction of the insulin/PI3K/Akt signaling pathway, which regulates glucose metabolism in the brain, can lead to tau hyperphosphorylation in the brain of AD patents. Additionally, insulin resistance in DM may cause β-amyloid (Aβ) deposition, which will be cleared by tau, but excessive phosphorylation of tau will further aggravate the neurotoxicity; then damage the brain and affect the cognitive function. GSK-3β is considered as a common kinase in insulin signaling transduction and tau protein phosphorylation, so we have reasons to believe that GSK-3β is a potential link between DM and AD.

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  • Impaired insulin secretion is multifactorial, the exact mechanism is still unclear, but commonly develops from glucose toxicity, lipid toxicity, immunoinflammatory response, and oxidative stress, leading to the dysfunction of islet β cells.

    “Impaired insulin secretion is multifactorial, the exact mechanism is still unclear, but commonly develops from glucose toxicity, lipid toxicity, immunoinflammatory response, and oxidative stress, leading to the dysfunction of islet β cells (72).”

    From Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments (2020) · cites this paper as [72]

  • When the insulin signaling pathway fails, the expression of GSK3β improves, which reduces the insulin sensitivity and increases the levels of blood glucose, thus subsequently leading to type 2 diabetes.

    “When the insulin signaling pathway fails, the expression of GSK3β improves, which reduces the insulin sensitivity and increases the levels of blood glucose, thus subsequently leading to T2D (72, 96, 97).”

    From Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments (2020) · cites this paper as [72]

  • Impairment of insulin signaling induces increased activation of GSK-3β, which phosphorylates Tau, leading to Tau hyperphosphorylation.

    “In addition, the impairment of insulin signaling induces an increased activation of GSK-3β, which phosphorylates Tau, hence leading to Tau hyperphosphorylation (Hong and Lee, 1997; Planel et al., 2007; Zhang et al., 2018; Wei et al., 2021).”

    From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Zhang et al., 2018

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Authors
Zhang, Y., Huang, N.-Q., Yan, F., Jin, H., Zhou, S.-Y., Shi, J.-S., & Jin, F.
Affiliations
Zunyi Medical University (CN)
Corresponding author
  • Jin, Hai
  • Jin, Feng
ORCID
Venue
Behavioural Brain Research
Publisher
Elsevier BV
Published
2018-02
Volume
339
Pages
57-65
ISSN
0166-4328 (ISSN-L)
DOI
10.1016/j.bbr.2017.11.015
OpenAlex
W2770586248
Cited by
301
References
130
Citations by year
2026: 28 · 2025: 38 · 2024: 45 · 2023: 48 · 2022: 42 · 2021: 38 · 2020: 37 · 2019: 14 · 2018: 10
FWCI
2.05
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Behavioural Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (81660599, 81360311, 81460548)
  • Postgraduate Education Foundation of Guizhou Province (KYJJ2017008)
  • Zunyi Medical University Funds (2013F-686, F-738)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Aldose Reductase and Taurine
Keywords
diabetes mellitus, Alzheimer's disease, glycogen synthase kinase-3β, type 3 diabetes, insulin resistance, tau hyperphosphorylation, amyloid-beta deposition, glycogen synthesis, neurotoxicity
MeSH terms
Glycogen Synthase Kinase 3 beta, Alzheimer Disease, Animals, Diabetes Mellitus, Humans, Insulin, Amyloid beta-Peptides, tau Proteins

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