| Residential College | true |
| Status | 已發表Published |
| Artemisinin diminished the hyperphosphorylation of Tau induced by Aβ1-42 via the AKT/GSK-3β pathway in vitro and in vivo Alzheimer's disease modle | |
Yitian Chen; Wenhua Zheng 
| |
| 2024-06 | |
| Conference Name | The 10th Macau Symposium on Biomedical Science |
| Conference Date | 2024-06-13-15 |
| Conference Place | University of Macau,University Hall |
| Abstract | Alzheimer's disease (AD) is the most common neuronal degenerative disease with a latent onset. It is mainly characterized by progressive memory loss and cognitive dysfunction. The etiology of AD is unknown, and multiple hypotheses have been proposed. AD is pathologically characterized by amyloid plaques, neurofibrillary tangles and loss of synapses and neurons. Amyloid-β (Aβ) peptide and hyperphosphorylated tau are the primary components of the plaques and tangles, leading to brain neuronal death. We recently found that artemisinin, an anti-malarial drug, reduced Aβ deposit, and tau hyperphosphorylation, protected neuronal cells and improved cognitive function in Alzheimer's disease animal model-3xtg mice. However, the underlying mechanisms, especially the interactions between artemisinin, Aβ and tau phosphorylation, are unknown. In this project, we plan to study the effect of Aβ and Artemisinin on tau phosphorylation in vitro and in vivo animal models and the underlying mechanisms. Our preliminary data showed that Aβ increased the phosphorylation of tau in PC12 cells and caused cell apoptosis, while artemisinin alleviated the effects of Aβ. Western blots showed that Aβ increased phosphorylation of Tau at sites of Ser 396 and 404, Thr 181 and 231 in PC12 cells, while artemisinin activated AKT kinase by stimulating the phosphorylation of the ser 473 sites of AKT in PC12 cells, leading to the phosphorylation of the ser 9 of GSK-3β and the inhibition of GSK-3β, ultimately reducing tau hyperphosphorylation and protecting PC12 cell from Aβ injury. Similar results were obtained in SY5Y neuronal cells. In the 3xTG mice model, artemisinin alleviated memory deficit and cognitive dysfunction and reduced tau phosphorylation. In future studies, we will further investigate the effect of artemisinin on tau phosphorylation and underlying mechanisms in vivo. Our findings will contribute to understanding the interactions among the Artemisinin, Aβ and tau phosphorylation, and provide evidence that artemisinin may be a potential new drug for the treatment of AD in the clinic. |
| Other Abstract | Funds: Supported by National Natural Science Foundation of China (32070969), The Science and Technology Development Fund, Macau SAR (File No. 0127/2019/A3, 0113/2018/A3 and 0038/2020/AMJ), The Guangdong Provincial Funding Committee for Basic and Applied Fundamental Research (2022-Natural Science Foundation), University of Macau (File No. MYRG2018-00134-FHS and MYRG2020-00158-FHS). |
| Keyword | Alzheimer’s Disease, Aβ, Tau Hyperphosphorylation, Artemisinin, Gsk-3β, P13k/akt |
| Document Type | Conference paper |
| Collection | DEPARTMENT OF PHARMACEUTICAL SCIENCES |
| Corresponding Author | Wenhua Zheng |
| Recommended Citation GB/T 7714 | Yitian Chen,Wenhua Zheng. Artemisinin diminished the hyperphosphorylation of Tau induced by Aβ1-42 via the AKT/GSK-3β pathway in vitro and in vivo Alzheimer's disease modle[C], 2024. |
| APA | Yitian Chen., & Wenhua Zheng (2024). Artemisinin diminished the hyperphosphorylation of Tau induced by Aβ1-42 via the AKT/GSK-3β pathway in vitro and in vivo Alzheimer's disease modle. . |
| Files in This Item: | There are no files associated with this item. | |||||
Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.
Edit Comment