We report here that (1) AURKA phosphorylation was decreased in the human AD brain, (2) pharmacological activation of AURKA increased AURKA phosphorylation, acidified endolysosomes, decreased the activity of BACE-1, increased the activity of cathepsin D, and decreased intracellular and secreted levels of Aβ1-40 and Aβ1-42, and (3) pharmacological inhibition of AURKA decreased AURKA phosphorylation, de-acidified endolysosomes, decreased the activity of cathepsin D, and increased intracellular and secreted levels of Aβ1-40 and Aβ1-42. The gene discussed is BACE1; the disease is Alzheimer disease.