| First Author | Jin Y | Year | 2015 |
| Journal | Biochem Biophys Res Commun | Volume | 468 |
| Issue | 1-2 | Pages | 157-60 |
| PubMed ID | 26522221 | Mgi Jnum | J:233202 |
| Mgi Id | MGI:5780945 | Doi | 10.1016/j.bbrc.2015.10.141 |
| Citation | Jin Y, et al. (2015) Amyloid-beta peptide increases cell surface localization of alpha7 ACh receptor to protect neurons from amyloid beta-induced damage. Biochem Biophys Res Commun 468(1-2):157-60 |
| abstractText | Amyloid-beta peptide 1-42 (Abeta1-42) reduced PC-12 cell viability in a concentration (1-10 muM)- and treatment time (48-72 h)-dependent manner. Nicotine prevented Abeta1-42-induced PC-12 cell death, but conversely, the alpha7 ACh receptor antagonist alpha-bungarotoxin enhanced Abeta1-42-induced cell toxicity. Extracellularly applied Abeta1-42 significantly increased cell surface localization of alpha7 ACh receptor in PC-12 cells as compared with that for non-treated control cells. Cell surface localization of alpha7 ACh receptor in the brain of 5xFAD mouse, an animal model of Alzheimer's disease (AD), apparently increased in an age (1-12 months)-dependent manner in association with increased accumulation of Abeta1-42 in the plasma membrane component. Taken together, these results indicate that Abeta1-42 promotes translocation of alpha7 ACh receptor towards the cell surface and that alpha7 ACh receptor rescues neuronal cells from Abeta1-42-induced damage. |
