The compound, which had already been tested on age-related learning and memory impairment in mice [184], was administered to triple-transgenic Alzheimer’s disease (3xTg-AD) mice that expressed mutant forms of the amyloid-protein precursor and presenilin 1 (found in hereditary forms of Alzheimer’s disease), and a mutated form of the microtubule-associated protein tau (associated with frontal temporal dementia) [287]. The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.