Evidence mapPaperPMID 40905109Full record

ArticleCNS neuroscience & therapeutics2025

ApoE4 Upregulates GSK-3β to Aggravate Alzheimer-Like Pathologies and Cognitive Impairment in Type 2 Diabetic Mice.

Yuying Wang, Yang Gao, Yarong Wang, Fuqiang Zhang, Fei Sun, Xin Wang, Jiazhao Xie, Zhipeng Xu, Junjian Zhang, Haibo Xu and 2 more

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Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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4citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Yuying WangKey Laboratory of Ministry of Education for Neurological Disorders, Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0009-0006-1741-3559
Yang GaoDepartment of Radiology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.ORCID 0000-0003-1707-9053
Yarong WangKey Laboratory of Ministry of Education for Neurological Disorders, Department of Endocrine, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fuqiang ZhangKey Laboratory of Ministry of Education for Neurological Disorders, Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fei SunKey Laboratory of Ministry of Education for Neurological Disorders, Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xin WangKey Laboratory of Ministry of Education for Neurological Disorders, Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jiazhao XieKey Laboratory of Ministry of Education for Neurological Disorders, Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zhipeng XuDepartment of Neurology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Junjian ZhangDepartment of Neurology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Haibo XuDepartment of Radiology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.ORCID 0000-0002-8451-8979
Yao ZhangKey Laboratory of Ministry of Education for Neurological Disorders, Department of Endocrine, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jian-Zhi WangKey Laboratory of Ministry of Education for Neurological Disorders, Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Funding

China Postdoctoral Science Foundation General Program 2024M762504Guangdong Provincial Key S&T Program 2018B030336001National Natural Science Foundation of China 31730035National Natural Science Foundation of China 81721005National Natural Science Foundation of China 91949205
6 · The paper itself

Abstract

backgroundThe apolipoprotein E (ApoE) ε4 allele and type 2 diabetes mellitus (T2DM) are independent risk factors for Alzheimer's disease (AD), the most prevalent neurodegenerative disorder in the elderly. The T2DM patients carrying the ApoE ε4 allele exhibit heightened activation of platelet glycogen synthase kinase-3β (GSK-3β), a key downstream kinase in the insulin signaling pathway, along with more severe cognitive deficits. This observation suggests an intrinsic link between ApoE ε4, GSK-3β, and cognitive dysfunction. However, the precise mechanisms by which ApoE ε4 influences GSK-3β activity and exacerbates brain pathology and cognitive decline in T2DM patients remain poorly understood.

methodsTo investigate these mechanisms, we developed T2DM mouse models by generating humanized ApoE ε3/ε3 and ε4/ε4 knock-in mice. The mice were subjected to a high-fat diet combined with multiple low-dose intraperitoneal streptozotocin injections to induce T2DM. We then assessed GSK-3β expression, AD-like pathologies, and cognitive functions in these models.

resultsWe observed that GSK-3β activity was significantly upregulated in ApoE4 mice, accompanied by disruption of the insulin signaling pathway. Notably, ApoE4-T2DM mice exhibited exacerbated AD-related pathologies, including increased accumulation of hyperphosphorylated tau, neuroinflammation, and synaptic loss. These changes were correlated with more severe cognitive impairments compared with ApoE3-T2DM or ApoE4 mice. Furthermore, inhibition of GSK-3β activity using the selective inhibitor 9-ING-41 effectively ameliorated both AD-like pathologies and cognitive deficits in ApoE4-T2DM mice.

conclusionsOur findings suggest that ApoE4 exacerbates AD pathogenesis by activating GSK-3β. Furthermore, targeting GSK-3β may offer a promising therapeutic strategy to halt the progression from T2DM to AD, providing new insights into potential interventions for patients at risk.

Indexed as

Alzheimer DiseaseApolipoprotein E4Cognitive DysfunctionDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Glycogen Synthase Kinase 3 betaAnimalsDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMice, Transgenictau ProteinsUp-RegulationApolipoprotein E4Glycogen Synthase Kinase 3 betaGsk3b protein, mousetau Proteins9‐ING‐41Alzheimer's diseaseApoEglycogen synthase kinase‐3βtype 2 diabetes mellitus

Identifiers

PMID40905109
PMCPMC12409304

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.