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Type: Journal article
Title: Edaravone alleviates Alzheimer's disease-type pathologies and cognitive deficits
Author: Jiao, S.S.
Yao, X.Q.
Liu, Y.H.
Wang, Q.H.
Zeng, F.
Lu, J.J.
Liu, J.
Zhu, C.
Shen, L.L.
Liu, C.H.
Wang, Y.R.
Zeng, G.H.
Parikh, A.
Chen, J.
Liang, C.R.
Xiang, Y.
Bu, X.L.
Deng, J.
Li, J.
Xu, J.
et al.
Citation: Proceedings of the National Academy of Sciences of the United States of America, 2015; 112(16):5225-5230
Publisher: National Academy of Sciences
Issue Date: 2015
ISSN: 0027-8424
Statement of
Shu-Sheng Jiao, Xiu-Qing Yao, Yu-Hui Liu, Qing-Hua Wang, Fan Zeng, Jian-Jun Lu ... et al.
Abstract: Alzheimer's disease (AD) is one of most devastating diseases affecting elderly people. Amyloid-β (Aβ) accumulation and the downstream pathological events such as oxidative stress play critical roles in pathogenesis of AD. Lessons from failures of current clinical trials suggest that targeting multiple key pathways of the AD pathogenesis is necessary to halt the disease progression. Here we show that Edaravone, a free radical scavenger that is marketed for acute ischemic stroke, has a potent capacity of inhibiting Aβ aggregation and attenuating Aβ-induced oxidation in vitro. When given before or after the onset of Aβ deposition via i.p. injection, Edaravone substantially reduces Aβ deposition, alleviates oxidative stress, attenuates the downstream pathologies including Tau hyperphosphorylation, glial activation, neuroinflammation, neuronal loss, synaptic dysfunction, and rescues the behavioral deficits of APPswe/PS1 mice. Oral administration of Edaravone also ameliorates the AD-like pathologies and memory deficits of the mice. These findings suggest that Edaravone holds a promise as a therapeutic agent for AD by targeting multiple key pathways of the disease pathogenesis.
Keywords: Alzheimer’s disease; Edaravone; amyloid-β; BACE1; oxidative stress
Rights: Freely available online through the PNAS open access option
RMID: 1000033651
DOI: 10.1073/pnas.1422998112
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Appears in Collections:Medicine publications

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