Exploring the Diverse Roles of GSK-3β Kinase in Alzheimer’s Disease

Alzheimer’s disease, a progressive neurodegenerative disorder, is a global health concern whose consequence affects an individual’s cognitive scores, behavioral patterns, mood swings, and psychology. Globally, the condition is prevalent among elderly population groups. The inclusion of fibrillary lesions (NFTs) and senile plaques (Aβ) constitutes two contentious diagnostic factors contributing to AD-related deterioration. A compendium of continual mistranslated dialogs among several protein kinases, phosphatases, and transcription factors leads to misinterpreted signaling, thus forming the early manifestations of the condition. Neurodegenerative disorders, such as Alzheimer’s disease, have been linked to abnormalities in biochemical signals. Glycogen synthase kinase-3 (GSK-3) is a widely acknowledged regulator engaging in the formation and subsequent advance-ment of AD pathophysiology along with controlling several critical targets involving neuronal deterioration. Consequently, they are regarded as a critical region of interest in the disease-modifying diagnosis of Alzheimer’s disease (AD), where anomalous expression of this enzyme has indeed been implicated with overexpression of Aβ peptide, further initiating a cascade sequence leading to hyperphosphorylation of tau proteins. Hence, the focus on elucidating potential GSK-3 inhibitors aids in halting the disease progress and helps us observe the interlinking among several mechanisms of cellular functions involving GSK-3. This review ascertains the in-depth knowledge regarding GSK-3 and summarizes the surrounding elements responsible for alleviating its negative impact in patho-logical conditions. Along with it, we highlight the emergence of several clinical therapeutics and their studies to observe the potentials of GSK-3 inhibitors and assist our commands in understanding their effects on AD targets.