• Jing-Yi Liu, Xiao-Xin Chen, Hai-Yong Chen, Jun Shi, George Pak-Heng Leung, Sydney Chi-Wai Tang, Li-Xing Lao, Henry Ka-Fun Yip, Kai-Fai Lee, Stephen Cho-Wing Sze, Zhang-Jin Zhang, and Kalin Yanbo Zhang.
• School of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
• Neuroscience. 2018 Dec 1; 394: 72-82.

AbstractAlzheimer's disease (AD) is the most common cause of dementia in the elderly, characterized by progressive cognitive dysfunction. Aquaporin 9 (AQP9) is an aquaglyceroporin membrane channel shown biophysically to conduct water, glycerol, and other small solutes. In our study, we reported for the first time an age-associated decrease in AQP9 mRNA and protein expressions in both hippocampus and cerebral cortex of APPswe/PS1dE9 (Tg) AD mice at 3, 6 and 10 months of age. Consistently, we observed a dose-dependent downregulation of AQP9 expression in PC12 cells after treatment with amyloid-beta protein 1-40 (Aβ1-40). Pre-treatment with AQP9 small interfering RNA led to a more severe neurotoxicity in PC12 cells in response to Aβ1-40. Furthermore, we corroborated that the active participation of AQP9 in AD progression is associated with Aβ-induced apoptosis both in vitro and in vivo. Taken together, our results reveal an important role of AQP9 in Aβ-induced pathogenesis of AD which deserves further investigation.Copyright © 2018. Published by Elsevier Ltd.

37 keywords...

hide…