Unraveling the Role of the Glycogen Synthase Kinase-3β, Bruton's Tyrosine Kinase, and Sphingosine 1 Phosphate Pathways in Multiple Sclerosis.

Inflammation, demyelination, and neurodegeneration are symptoms of the central nervous system (CNS) condition known as Multiple sclerosis (MS). Due to its crucial function in controlling immune cell activation and inflammation, the glycogen synthase kinase-3β (GSK- 3β), Bruton's tyrosine kinase (BTK), and Sphingosine 1 phosphate (S1P) signaling pathway have become a viable target for the therapy of MS. The GSK-3β signaling system, which controls several biological target processes, including cell survival, proliferation, and inflammation, depends on the GSK-3β enzyme. In MS animal models and human studies, GSK-3β inhibition has been demonstrated to lessen demyelination and inflammation. Clinical research on MS has demonstrated that BTK inhibitors decrease inflammation and disease activity by preventing B cell activation and the subsequent release of cytokines. Clinical investigations for MS have demonstrated that S1P modulators, such as fingolimod, lower disease activity and inflammation by limiting immune cell migration to the central nervous system and preventing cytokine production. The GSK-3β /BTK/S1P signaling pathway in MS is the subject of this paper's summary and discussion of prospective treatment targets.