Publication

Bilateral Implantation of Shear Stress Modifier in ApoE Knockout Mouse Induces Cognitive Impairment and Tau Abnormalities

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Last modified
  • 05/15/2025
Type of Material
Authors
    Keqiang Ye, Emory UniversityZhentao Zhang, Emory UniversityGuiqin Chen, Emory UniversityJing Xiong, Emory UniversityS Nie, Wuhan UniversityY Tan, Huazhong University of Science & TechnologyD Hu, Wuhan UniversityX Cao, Huazhong University of Science & Technology
Language
  • English
Date
  • 2018-10-04
Publisher
  • Frontiers Media
Publication Version
Copyright Statement
  • © 2018 Nie, Tan, Zhang, Chen, Xiong, Hu, Ye, Zhang, Cao, Chen and Zhang.
License
Final Published Version (URL)
Title of Journal or Parent Work
ISSN
  • 1663-4365
Volume
  • 10
Issue
  • OCT
Start Page
  • 303
End Page
  • 303
Grant/Funding Information
  • This study was supported by the Johns Hopkins School of Medicine startup fund to LC; National Natural Science Foundation of China (NSFC Project No. 81701257 and No. 81671051) and the Foundation of Independent Research Projects of Wuhan University (2042017kf0050) to SN and Z-HZ.
Abstract
  • Vascular cognitive impairment (VCI) encompasses all causes of cerebrovascular disease that lead to cognitive decline, or overt dementia, atherosclerotic disease being the most common contributor. However, few rodent models that mimic the pathology of VCI replicated the clinical cerebrovascular atherosclerosis. Here we aimed to investigate the mechanism underlying VCI in an Apolipoprotein E knockout (ApoE-KO) mouse model fed with western style food with implantation of bilateral shear stress modifiers. We established a cognitive decline in spatial learning and memory developed in the bilateral modifier treated mice. Brain imaging and pathological examinations demonstrated reduced glucose intake and neuronal loss in hippocampus. Although no amyloid plaques or neurofibrillary tangles (NFTs) were observed, tau pathology including hyperphosphorylation, paired helical filament formation and pathologic truncation were found at considerable higher extent in the bilateral modifier group 8 weeks post the procedure. In addition, gliosis and microglia activation were confirmed in corpus callosum (CC) and ventral striatum. Thus, this ApoE-KO mouse model faithfully replicates the stenosis of common carotid artery (CCA) and cognitive impairment following atherosclerotic deposition and global cerebral hypoperfusion. The close correlation of cognitive decline and tau pathology indicates the toxic tau species could be at least partially responsible for the neurodegenerative changes induced by the chronic hypoxia/ischemia.
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Research Categories
  • Health Sciences, Pathology

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