To protect the glutamatergic components from damage caused by AD, Qian et al. [163] screened five bioactive compounds including propyl cinnamate, methyl cinnamate, procyanidin B1, procyanidin B2 and myristicin as the brain synapse-targeting active substances, identifying GABA pathway with γ-aminobutyric acid type A receptor subunit gamma 2 (GABRG2), GABA receptor alpha1 subunit (GABRA1), GABA receptor beta 2 subunit (GABRB2), and GABA receptor alpha 5 subunit (GABRA5) as the core therapeutic targets of cinnamon against AD-related GABAergic synaptic dysfunction. This evidence concerns the gene GABRG2 and Alzheimer disease.