Indirubin-3'-monoxime rescues spatial memory deficits and attenuates beta-amyloid-associated neuropathology in a mouse model of Alzheimer's disease.

作者: Yun Ding , Aimin Qiao , Guo-Huang Fan

DOI: 10.1016/J.NBD.2010.03.022

关键词:

摘要: Indirubin and its derivatives have been shown to possess potent inhibitory effects on cyclin-dependent protein kinase 5 glycogen synthase 3beta, two kinases involved in abnormal hyperphosphorylation of tau amyloid precursor processing/beta-amyloid (Abeta) production. Here, we showed that systemic treatment APP presenilin 1 (PS1) transgenic mice, a robust Alzheimer's disease (AD) mouse model, with indirubin-3'-monoxime (IMX; 20mg/kg; 3 times weekly), for as little 2months, significantly attenuated spatial memory deficits. This was accompanied by marked decrease several AD-like phenotypes, including Abeta deposition, hyperphosphorylation, accumulation activated microglia astrocytes around plaques, loss synaptophysin immunoreactivity. These findings suggest IMX is potential therapeutic agent combat AD.

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