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He Z, Han S, Zhu H, et al. The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer's Disease in APPSwe/PS1dE9 Mice. Front Mol Neurosci. 2020;13:21doi: 10.3389/fnmol.2020.00021.
He, Z., Han, S., Zhu, H., Hu, X., Li, X., Hou, C., Wu, C., Xie, Q., Li, N., Du, X., Ni, J., & Liu, Q. (2020). The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer's Disease in APPSwe/PS1dE9 Mice. Frontiers in molecular neuroscience, 1321. https://doi.org/10.3389/fnmol.2020.00021
He, Zhijun, et al. "The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer's Disease in APPSwe/PS1dE9 Mice." Frontiers in molecular neuroscience vol. 13 (2020): 21. doi: https://doi.org/10.3389/fnmol.2020.00021
He Z, Han S, Zhu H, Hu X, Li X, Hou C, Wu C, Xie Q, Li N, Du X, Ni J, Liu Q. The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer's Disease in APPSwe/PS1dE9 Mice. Front Mol Neurosci. 2020 Mar 10;13:21. doi: 10.3389/fnmol.2020.00021. eCollection 2020. PMID: 32210760; PMCID: PMC7077345.
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Front Mol Neurosci. 2020 Mar 10;13:21. doi: 10.3389/fnmol.2020.00021. eCollection 2020.

The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer's Disease in APPSwe/PS1dE9 Mice.

Frontiers in molecular neuroscience

Zhijun He, Shuangxue Han, Huazhang Zhu, Xia Hu, Xiaoqian Li, Chaofan Hou, Chong Wu, Qingguo Xie, Nan Li, Xiubo Du, Jiazuan Ni, Qiong Liu

Affiliations

  1. Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, China.
  2. College of Optoelectronics Engineering, Shenzhen University, Shenzhen, China.
  3. College of Life Science, Huazhong University of Science and Technology, Wuhan, China.

PMID: 32210760 PMCID: PMC7077345 DOI: 10.3389/fnmol.2020.00021

Abstract

Alzheimer's disease (AD) is a widely distributed neurodegenerative disease characterized clinically by cognitive deficits and pathologically by formation of amyloid-β (Aβ) plaque and neurofibrillary tangles (NFTs) in the brain. Vanadium is a biological trace element that has a function to mimic insulin for diabetes. Bis(ethylmaltolato) oxidovanadium (IV) (BEOV) has been reported to have a hypoglycemic property, but its effect on AD remains unclear. In this study, BEOV was supplemented at doses of 0.2 and 1.0 mmol/L to the AD model mice APPSwe/PS1dE9 for 3 months. The results showed that BEOV substantially ameliorated glucose metabolic disorder as well as synaptic and behavioral deficits of the AD mice. Further investigation revealed that BEOV significantly reduced Aβ generation by increasing the expression of peroxisome proliferator-activated receptor gamma and insulin-degrading enzyme and by decreasing β-secretase 1 in the hippocampus and cortex of AD mice. BEOV also reduced tau hyperphosphorylation by inhibiting protein tyrosine phosphatase-1B and regulating the pathway of insulin receptor/insulin receptor substrate-1/protein kinase B/glycogen synthase kinase 3 beta. Furthermore, BEOV could enhance autophagolysosomal fusion and restore autophagic flux to increase the clearance of Aβ deposits and phosphorylated tau in the brains of AD mice. Collectively, the present study provides solid data for revealing the function and mechanism of BEOV on AD pathology.

Copyright © 2020 He, Han, Zhu, Hu, Li, Hou, Wu, Xie, Li, Du, Ni and Liu.

Keywords: Alzheimer’s disease; amyloid beta (Aβ); autophagy; bis(ethylmaltolato) oxidovanadium (IV) (BEOV); peroxisome proliferator-activated receptor gamma (PPARγ); protein tyrosine phosphatase-1B (PTP1B); vanadium

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