In animal models, using an amyloid precursor protein (APP)/presenilin-1 (PS-1) double transgenic (TG) mouse model of AD, treatment with QUET attenuated memory impairment, decreased the number of β-amyloid (Aβ) plaques and up-regulated the cerebral anti-apoptosis B-cell lymphoma (Bcl)-2 protein [18]. The gene discussed is PSEN1; the disease is Alzheimer disease.