| Effects |
(1)L1 mitigates the neuroinflammatory response of the activated microglia during the Aβ-induced inflammation process, (2)upon treatment of transgenic 5×FAD mice with L1 for 30 days, the level of amyloid plaques in the treated AD mouse brains was shown to decrease by up to 50% vs the vehicle-treated AD mouse brains, (3)L1 suppresses the p-tau aggregation near the amyloid plaques, as well as limits the activation of microglia near amyloid plaques by 30–44% vs the vehicle-treated AD mouse brains, (4)the L1-treated brain lysate vs the vehicle-treated control group(a 38% and 50% reduction for soluble and insoluble Aβ42 species, respectively) and a 49% reduction for the insoluble Aβ40 species, (5)L1 alleviates the neurotoxicity of Aβ aggregates and suppresses metal-mediated ROS generation and oxidative stress, which in turn leads to the attenuation of neuroinflammation mediated by activated microglia near the amyloid plaques, |
