Taken together, these results showed that mirodenafil has potential for use as a polypharmacological drug against AD pathology through the modulation of the cGMP/PKG/CREB pathway, Akt/GSK-3β-mediated phosphorylation of tau, GR transcriptional activity, Wnt/β-catenin signaling, and clearance of Aβ and tau. The gene discussed is CREB1; the disease is Alzheimer disease.