Consequently, the present study endeavors to experimentally induce an AD-like model via SCOP in mice and to examine the ability of TQ to enhance cognitive impairment and restoration of synaptic proteins through its PPAR-γ agonist activity with a particular focus on miR-9, which may lead to decreased deposition of amyloid β, the major hallmark of AD. The gene discussed is PPARG; the disease is Alzheimer disease.