In this respect, liraglutide injection for 4 weeks only mitigated the brain Aβ1–42 levels, without significantly affecting the Aβ1–40 or p-tau(Ser396) (a known intermediary phosphorylated residue in AD pathology [55,56]) in 3xTg-AD female mice with early AD-like pathology, which also presented less pronounced signs of motor, cognitive or synaptic defects (data not shown) (contrary to the previous observations of impaired motor activity and learning/memory in 3xTg-AD male mice [26,57]). The gene discussed is MAPT; the disease is Alzheimer disease.