ID | 57753 |
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Author |
Feng, Tian
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Yamashita, Toru
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Shang, Jingwei
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Shi, Xiaowen
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Nakano, Yumiko
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Morihara, Ryuta
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Tsunoda, Keiichiro
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Nomura, Emi
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Sasaki, Ryo
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Tadokoro, Koh
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Matsumoto, Namiko
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Hishikawa, Nozomi
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Kaken ID
Ohta, Yasuyuki
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Kaken ID
researchmap
Abe, Koji
Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Kaken ID
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Abstract | Alzheimer's disease (AD) and chronic cerebral hypoperfusion (CCH) often coexist in dementia patients in aging societies. The hallmarks of AD including amyloid-β (Aβ)/phosphorylated tau (pTau) and pathology-related events such as neural oxidative stress and neuroinflammation play critical roles in pathogenesis of AD with CCH. A large number of lessons from failures of drugs targeting a single target or pathway on this so complicated disease indicate that disease-modifying therapies targeting multiple key pathways hold potent potential in therapy of the disease. In the present study, we used a novel mouse model of AD with CCH to investigate a potential therapeutic effect of a free radical scavenger, Edaravone (EDA) on AD with CCH via examining motor and cognitive capacity, AD hallmarks, neural oxidative stress, and neuroinflammation. Compared with AD with CCH mice at 12 months of age, EDA significantly improved motor and cognitive deficits, attenuated neuronal loss, reduced Aβ/pTau accumulation, and alleviated neural oxidative stress and neuroinflammation. These findings suggest that EDA possesses clinical and pathological benefits for AD with CCH in the present mouse model and has a potential as a therapeutic agent for AD with CCH via targeting multiple key pathways of the disease pathogenesis.
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Keywords | Alzheimer’s disease
chronic cerebral hypoperfusion
edaravone
neural oxidative stress
neuroinflammation
neuronal loss
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Note | The final publication is available at IOS Press through https://doi.org/10.3233/JAD-190369
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Published Date | 2019-09-03
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Publication Title |
Journal of Alzheimer's Disease
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Volume | volume71
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Issue | issue1
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Publisher | IOS Press
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Start Page | 327
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End Page | 339
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ISSN | 1387-2877
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NCID | AA11545428
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Content Type |
Journal Article
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language |
English
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OAI-PMH Set |
岡山大学
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File Version | author
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Related Url | isVersionOf https://doi.org/10.3233/JAD-190369
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