Multiple network analysis, including compound-target and target-function analyses, followed by experimental validation demonstrated the therapeutic effects of BSYZ on cognitive dysfunction in APP/PS1 mice (a double transgenic mice with neurons expressing a chimeric mouse/human amyloid precursor protein and a mutant human presenilin 1; both mutations are associated with early-onset Alzheimer’s disease), possibly via regulating amyloid-β metabolism and suppressing neuronal apoptosis (Cai et al., 2018; Table 1). This evidence concerns the gene APP and Alzheimer disease.