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Dysregulation of GSK-3\u03b2 kinase has been reported in diabetes, cancer, Alzheimer\u2019s disease, schizophrenia, bipolar disorder, inflammation, and Huntington\u2019s disease. Thus, GSK-3\u03b2 is widely regarded as a promising target for therapeutic use. The current review article focuses mainly on Alzheimer\u2019s disease, an age-related neurodegenerative brain disorder. GSK-3\u03b2 activation increases amyloid-beta (A\u03b2) and the development of neurofibrillary tangles that are involved in the disruption of material transport between axons and dendrites. The drug-binding cavities of GSK-3\u03b2 are explored, and different existing classes of GSK-3\u03b2 inhibitors are explained in this review. Non-ATP competitive inhibitors, such as allosteric inhibitors, can reduce the side effects compared to ATP-competitive inhibitors. Whereas ATP-competitive inhibitors produce disarrangement of the cytoskeleton, neurofibrillary tangles formation, and lead to the death of neurons, etc. This could be because they are binding to a site separate from ATP. Owing to their interaction in particular and special binding sites, allosteric ligands interact with substrates more selectively, which will be beneficial in resolving drug-induced resistance and also helpful in reducing side effects. 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