CREB1 and Alzheimer disease: Mirodenafil treatment significantly enhanced cGMP levels, and ameliorated CREB/BDNF signaling (CREB phosphorylation, NGF and BDNF expression), abnormal protein aggregation (Aβ and hyperphosphorylated tau), mitochondrial membrane potential, apoptosis (caspase-3 and PARP levels), autophagy (LC3B)-II and p62 expression), phosphorylation of kinases [GSK-3β, Akt and AMPK], and expression of AD-associated genes including APP and BACE1 in neuronal cells treated with Aβ1-42 [18].