For the AD model, we used a previously described animal model of focal DTR (diphtheria receptor)-expressing astrocytes in APP/PS1 mice (fGiD).12 This approach addresses the limitations of APP/PS1, which exhibits amyloid pathology but minimal global neurodegeneration,37 by inducing severe reactive astrocytes to precipitate neuronal death.12 Behavioral assessments, including the PAT and novel place recognition (NPR)38 tests, revealed memory and cognitive impairments in fGiD mice, which were significantly reversed by KDS12025 (3 mg/kg/day, 16 times, intraperitoneal injection) (Fig. 4a–c). The gene discussed is APP; the disease is amyloidosis.