The Role of Glycogen Synthase Kinase 3 Beta in Neuroinflammation and Pain

Neuroinflammation is a crucial mechanism related to many neurological diseases. Extensive studies in recent years have indicated that dysregulation of Glycogen Synthase Kinase 3 Beta (GSK3β) contributes to the development and progression of these disorders through regulating the neuroinflammation processes. Inhibitors of GSK3β have been shown to be beneficial in many neuroinflammatory disease models including Alzheimer’s disease, multiple sclerosis and AIDS dementia complex. Glial activation and elevated pro-inflammation cytokines (signs of neuroinflammation) in the spinal cord have been widely recognized as a pivotal mechanism underlying the development and maintenance of many types of pathological pain. The role of GSK3β in the pathogenesis of pain has recently emerged. In this review, we will first assess the GSK3β structure, regulation, and mechanisms by which GSK3β regulates inflammation. We will then describe neuroinflammation in general and in specific types of neurological diseases and the potential beneficial effects induced byinhibiting GSK3β. Finally, we will provide new evidence linking aberrant levels of GSK3β in the development of pathological pain.