In AD mice, β-amyloid (Aβ), one of the typical pathological features of this disease, can decrease the BDNF content in the hippocampus [15]; this occurs mostly by lowering phosphorylated cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) levels, downstream of and regulated via phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) pathways [16]. The gene discussed is CREB1; the disease is Alzheimer disease.