The use of three murine genetic models of Alzheimer's disease reveals efficacy of 4',5,7-trihydroxyisoflavone in alleviating cognitive deficits and reducing levels of amyloid-beta and hyperphosphorylated tau protein

Background

Despite intensive studies on developing therapies for Alzheimer's disease (AD), there is still a need to improve the treatment efficacy. Results of recent studies indicated that genistein (4',5,7-trihydroxyisoflavone) was effective in an autophagy stimulation-dependent improving of cognitive deficits and reducing levels of amyloid-beta and hyperphosphorylated tau protein in brains, when employing a streptozotocin-induced rat model of the sporadic form of AD. Despite those encouraging results, the above-mentioned model has its limitations, mainly related to the rapid and inducible character of the symptoms caused by streptozotocin, induction of other effects (like diabetes) by this toxin, and the requirement for invasive administration of this compound to the brain, in contrast to naturally occurring AD. Thus, in this study, we hypothesized that genistein might be effective in reducing symptoms of AD in well-defined genetic models of this disease and tested the efficacy of this compound.