Administration of Sch B significantly inhibits glycogen synthase kinase 3β (GSK3β) activation in the hippocampus and cortex neurons of triple-transgenic Alzheimer’s disease (3 × Tg AD) mice, upregulates Nrf2, GPX4, and ferroptosis suppressor protein 1 (FSP1) expression, reduces levels of MDA, Fe2+, ROS, and tumor necrosis factor alpha (TNF-α), thereby suppressing neuronal ferroptosis and neuroinflammation and improving learning and memory performance. Here, GSK3B is linked to Alzheimer disease.