In AD research, OST exhibits multiple benefits besides antagonizing microglial activation, including (1) decreasing Aβ cytotoxicity on neural cells by mediating phosphorylation of cAMP response element-binding protein (CREB) [30], (2) inhibiting apoptosis by mediating Wnt/β-catenin signaling [31], (3) improving synaptic plasticity and cognitive function by regulating the glutamatergic neuron [32], and (4) increasing hippocampal neurogenesis by upregulating Bdnf in AD mice [33]. This evidence concerns the gene CREB1 and Alzheimer disease.