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


ABSTRACT: 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 (GSK3?) contributes to the development and progression of these disorders through regulating the neuroinflammation processes. Inhibitors of GSK3? have been shown to be beneficial in many neuroinflammatory disease models including Alzheimer's disease, multiple sclerosis and AIDS dem entia 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 GSK3? in the pathogenesis of pain has recently emerged. In this review, we will first review the GSK3? structure, regulation, and mechanisms by which GSK3?regulates inflammation. We will then describe neuroinflammationin general and in specific types of neurological diseases and the potential beneficial effects induced by inhibiting GSK3?. Finally, we will provide new evidence linking aberrant levels of GSK3? in the development of pathological pain.

SUBMITTER: Maixner DW 

PROVIDER: S-EPMC4193379 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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

Maixner Dylan Warren DW   Weng Han-Rong HR  

Journal of pharmaceutics & pharmacology 20130101 1


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 dem entia complex. Glial activation an  ...[more]

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