CB2R agonists consistently improve cognitive performance across various AD models, while also reducing Aβ deposition, oxidative stress, and inflammatory responses, with specific pathways such as peroxisome proliferator-activated receptor-γ (PPAR-γ), toll-like receptor 4 (TLR4)/NF-κB, and PI3K/Akt, implicated in these effects. The gene discussed is AKT1; the disease is Alzheimer disease.