Neuroprotective effect of formononetin in ameliorating learning and memory impairment in mouse model of Alzheimer's disease.
Biosci Biotechnol Biochem. 2018 Jan ;82(1):57-64. Epub 2017 Dec 1. PMID: 29191087
Alzheimer's disease (AD) is the most common cause of dementia among elderly population. Derangedβ-amyloid (Aβ) trafficking across the blood-brain barrier is known to be a critical element in the pathogenesis of AD. In the vascular endothelial cells of hippocampus, Aβ transport is mainly mediated by low-density lipoprotein-associated protein 1 (LRP1) and the receptor for advanced glycation end (RAGE) products; therefore, LRP1 and RAGE endothelial cells are potential therapeutic targets for AD. In this study, we explored the effects of Formononetin (FMN) on learning and memory improvement in APP/PS1 mice and the related mechanisms. We found that FMN significantly improved learning and memory ability by suppressing Aβ production from APP processing, RAGE-dependent inflammatory signaling and promoted LRP1-dependent cerebral Aβ clearance pathway. Moreover, FMN treatment alleviated ultrastructural changes in hippocampal vascular endothelial cells. In conclusion, we believe that FMNmay be an efficacious and promising treatment for AD.