| First Author | Wang SW | Year | 2016 |
| Journal | Behav Brain Res | Volume | 296 |
| Pages | 109-17 | PubMed ID | 26358659 |
| Mgi Jnum | J:227505 | Mgi Id | MGI:5700604 |
| Doi | 10.1016/j.bbr.2015.09.003 | Citation | Wang SW, et al. (2016) Alpha-tocopherol quinine ameliorates spatial memory deficits by reducing beta-amyloid oligomers, neuroinflammation and oxidative stress in transgenic mice with Alzheimer's disease. Behav Brain Res 296:109-17 |
| abstractText | The pathologies of Alzheimer's disease (AD) is associated with soluble beta-amyloid (Abeta) oligomers, neuroinflammation and oxidative stress. Decreasing the levels of Abeta oligomer, glial activation and oxidative stress are potential therapeutic approaches for AD treatment. We previously found alpha-tocopherol quinine (alpha-TQ) inhibited Abeta aggregation and cytotoxicity, decreased the release of inflammatory cytokines and reactive oxygen species (ROS) in vitro. However, whether alpha-TQ ameliorates memory deficits and other neuropathologies in mice or patients with AD remains unknown. In this study, we reported that orally administered alpha-TQ ameliorated memory impairment in APPswe/PS1dE9 transgenic mice, decreased oxidative stress and the levels of Abeta oligomer in the brains of mice, prevented the production of inducible nitric oxide synthase and inflammatory mediators, such as interleukin-6 and interleukin-1beta, and inhibited microglial activation by inhibiting NF-kappaB signaling pathway. These findings suggest that alpha-TQ has potential therapeutic value for AD treatment. |
