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Neuroprotective effects of salidroside through PI3K/Akt pathway activation in Alzheimer’s disease models

Authors Zhang B, Wang Y, Li H, Xiong R, Zhao Z, Chu X, Li Q, Sun S, Chen S

Received 5 November 2015

Accepted for publication 22 December 2015

Published 6 April 2016 Volume 2016:10 Pages 1335—1343

DOI https://doi.org/10.2147/DDDT.S99958

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Sumit Goswami

Peer reviewer comments 2

Editor who approved publication: Professor Wei Duan

Bei Zhang,1,2 Ying Wang,1 Hui Li,1 Ran Xiong,1 Zongbo Zhao,1 Xingkun Chu,2 Qiongqiong Li,1 Suya Sun,1 Shengdi Chen1,2

1Department of Neurology, Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China; 2Laboratory of Neurodegenerative Diseases, The Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China

Abstract: Alzheimer’s disease (AD) is a devastating neurodegenerative disorder characterized by deposits of aggregated amyloid-β (Aβ) peptide and neurofibrillary tangles in the brain parenchyma. Despite considerable research to elucidate the pathological mechanisms and identify therapeutic strategies for AD, effective treatments are still lacking. In the present study, we found that salidroside (Sal), a phenylpropanoid glycoside isolated from Rhodiola rosea L., can protect against Aβ-induced neurotoxicity in four transgenic Drosophila AD models. Both longevity and locomotor activity were improved in Sal-fed Drosophila. Sal also decreased Aβ levels and Aβ deposition in brain and ameliorated toxicity in Aβ-treated primary neuronal culture. The neuroprotective effect of Sal was associated with upregulated phosphatidylinositide 3-kinase (PI3K)/Akt signaling. Our findings identify a compound that may possess potential therapeutic benefits for AD and other forms of neurodegeneration.

Keywords: Alzheimer’s disease, amyloid-β, salidroside, Drosophila, neuroprotective effect

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