In the present study, SH-SY5Y human neuroblastoma cells were treated with GA, an inhibitor of glycolysis16, 17, and examinations of cell viability and measurements of the concentrations of Aβ42, total tau, and p-tauT181 proteins in culture media as well as the phosphorylation ratio of intracellular tau were then performed in order to determine the involvement of glucose metabolism in the pathophysiology of AD. The gene discussed is MAPT; the disease is Alzheimer disease.