Furthermore, the anti-inflammatory effects of MHDIs against Aβ-induced neuronal damage are partly attributable to the upregulation of BDNF/TrkB/ERK1/2-mediated signaling and downregulation of p38 MAPK/JNK-mediated signaling in the cortex and hippocampus in the early and late phases of AD in animal models (Table 4 and Figure 4). This evidence concerns the gene BDNF and Alzheimer disease.