Abstract :Alzheimer’s disease (AD) is a chronic neurodegenerative disease, responsible for dementia in 5.5 million Americans [1]. Accumulation of ß-amyloid (Aß) in the brain is a driving force behind AD neurodegenerative cascade and it is considered a prime target for disease modulatory therapy. Given that Aß accumulation precedes the onset of AD clinical symptoms by nearly two decades, therapeutics targeting Aß buildup likely will need to be applied over an extended period of time what requires from them a reasonable safety profile. A-directed immunotherapy and inhibitors of amyloid precursor protein (APP) proteases: ß-site cleaving enzyme 1 (BACE1) and ?-secretase complex (?-SC), which sequential action yields Aß, have been proposed as therapeutic approaches for AD. Unfortunately, thus far clinical trials of active Aß immunotherapy, anti-Aß monoclonal antibodies, and oral inhibitors of APP proteases conducted in AD subjects with mild and moderate dementia have encountered very limited success in improving cognitive metrics, while at the same time showed adverse effects specifically associated with each of these approaches [2-4].