Chronic 3,6′-DT administration ameliorates Aβ-induced neuroinflammation and microglial activation, preventing neurodegeneration and improving memory in an AD mouse model of stereotaxic intracerebroventricular Aβ1-42 [365] and reduces multiple hallmark features of AD, including glia activation, phosphorylated tau protein, APP, Aβ peptide, and Aβ-plaque number along cognitive dysfunction in 3×Tg-AD mice, and leads to synaptic preservation [363,366]. The gene discussed is APP; the disease is Alzheimer disease.