Protective effects of edaravone on white matter pathology in a novel mouse model of Alzheimer’s disease with chronic cerebral hypoperfusion

White matter lesions (WMLs) caused by cerebral chronic hypoperfusion (CCH) may contribute to the pathophysiology of Alzheimer’s disease (AD). However, the underlying mechanisms and therapeutic approaches have yet to be totally identified. In the present study, we investigated a potential therapeutic...

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Published in:Journal of cerebral blood flow and metabolism 2021-06, Vol.41 (6), p.1437-1448
Main Authors: Feng, Tian, Yamashita, Toru, Sasaki, Ryo, Tadokoro, Koh, Matsumoto, Namiko, Hishikawa, Nozomi, Abe, Koji
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cited_by cdi_FETCH-LOGICAL-c478t-6b77655199a919118b73e6d7a0ccf0f75fe840d55fa35ef159d12ca3f166263c3
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container_end_page 1448
container_issue 6
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container_title Journal of cerebral blood flow and metabolism
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creator Feng, Tian
Yamashita, Toru
Sasaki, Ryo
Tadokoro, Koh
Matsumoto, Namiko
Hishikawa, Nozomi
Abe, Koji
description White matter lesions (WMLs) caused by cerebral chronic hypoperfusion (CCH) may contribute to the pathophysiology of Alzheimer’s disease (AD). However, the underlying mechanisms and therapeutic approaches have yet to be totally identified. In the present study, we investigated a potential therapeutic effect of the free radical scavenger edaravone (EDA) on WMLs in our previously reported novel mouse model of AD (APP23) plus CCH with motor and cognitive deficits. Relative to AD with CCH mice at 12 months (M) of age, EDA strongly improved CCH-induced WMLs in the corpus callosum of APP23 mice at 12 M by improving the disruption of white matter integrity, enhancing the proliferation of oligodendrocyte progenitor cells, attenuating endothelium/astrocyte unit dysfunction, and reducing neuroinflammation and oxidative stress. The present study demonstrates that the long-term administration of EDA may provide a promising therapeutic approach for WMLs in AD plus CCH disease with cognitive deficits.
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title Protective effects of edaravone on white matter pathology in a novel mouse model of Alzheimer’s disease with chronic cerebral hypoperfusion
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