Alzheimer's disease (AD) is an extremely popular neurodegenerative condition associated with dementia, responsible for around 70% of the cases. There are presently 50 million people living with dementia in the world, but this number is anticipated to increase to 152 million by 2050, posing a substantial socioeconomic encumbrance. Despite extensive research, the precise mechanisms that cause AD remain unidentified, and currently, no therapy is available. Numerous signalling paths related to AD neuropathology, including glycogen synthase kinase 3-β (GSK-3β), have been investigated as potential targets for the treatment of AD in current years.GSK-3β is a proline-directed serine/threonine kinase that is linked to a variety of biological activities, comprising glycogen metabolism to gene transcription. GSK-3β is also involved in the pathophysiology of sporadic as well as familial types of AD, which has led to the development of the GSK3 theory of AD. GSK-3β is a critical performer in the pathology of AD because dysregulation of this kinase affects all the main symbols of the disease such as amyloid formation, tau phosphorylation, neurogenesis and synaptic and memory function. The current review highlights present-day knowledge of GSK-3β-related neurobiology, focusing on its role in AD pathogenesis signalling pathways. It also explores the possibility of targeting GSK-3β for the management of AD and offers an overview of the present research work in preclinical and clinical studies to produce GSK-3β inhibitors.
Keywords: Alzheimer’s disease; amyloid-beta; glycogen synthase kinase-3; glycogen synthase kinase-3 inhibitors; neurodegenerative diseases; tau protein.