The article discusses the role of glycogen synthase kinase 3 (GSK3) in the pathogenesis of Alzheimer's disease (AD). GSK3 is a serine/threonine kinase involved in various physiological processes, including glycogen metabolism, gene transcription, apoptosis, and microtubule stability. The authors propose the "GSK3 hypothesis of AD," suggesting that over-activity of GSK3 contributes to memory impairment, tau hyper-phosphorylation, increased β-amyloid production, and inflammatory responses, all of which are key features of AD. GSK3 activity is regulated by insulin and Wnt signaling pathways, and its dysregulation is linked to AD through alterations in these pathways. Evidence from cell culture, animal models, and human studies supports the role of GSK3 in AD, with increased GSK3 activity observed in AD brains. Inhibiting GSK3 activity has shown promising results in reversing some pathological effects in AD models, suggesting that GSK3 inhibitors could be a novel therapeutic approach for AD.The article discusses the role of glycogen synthase kinase 3 (GSK3) in the pathogenesis of Alzheimer's disease (AD). GSK3 is a serine/threonine kinase involved in various physiological processes, including glycogen metabolism, gene transcription, apoptosis, and microtubule stability. The authors propose the "GSK3 hypothesis of AD," suggesting that over-activity of GSK3 contributes to memory impairment, tau hyper-phosphorylation, increased β-amyloid production, and inflammatory responses, all of which are key features of AD. GSK3 activity is regulated by insulin and Wnt signaling pathways, and its dysregulation is linked to AD through alterations in these pathways. Evidence from cell culture, animal models, and human studies supports the role of GSK3 in AD, with increased GSK3 activity observed in AD brains. Inhibiting GSK3 activity has shown promising results in reversing some pathological effects in AD models, suggesting that GSK3 inhibitors could be a novel therapeutic approach for AD.