| First Author | Liu JY | Year | 2018 |
| Journal | Neuroscience | Volume | 394 |
| Pages | 72-82 | PubMed ID | 30266683 |
| Mgi Jnum | J:271512 | Mgi Id | MGI:6279461 |
| Doi | 10.1016/j.neuroscience.2018.09.016 | Citation | Liu JY, et al. (2018) Downregulation of Aquaporin 9 Exacerbates Beta-amyloid-induced Neurotoxicity in Alzheimer's Disease Models In vitro and In vivo. Neuroscience 394:72-82 |
| abstractText | Alzheimer'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 10months of age. Consistently, we observed a dose-dependent downregulation of AQP9 expression in PC12 cells after treatment with amyloid-beta protein 1-40 (Abeta1-40). Pre-treatment with AQP9 small interfering RNA led to a more severe neurotoxicity in PC12 cells in response to Abeta1-40. Furthermore, we corroborated that the active participation of AQP9 in AD progression is associated with Abeta-induced apoptosis both in vitro and in vivo. Taken together, our results reveal an important role of AQP9 in Abeta-induced pathogenesis of AD which deserves further investigation. |
