Title:Unraveling the Role of the Glycogen Synthase Kinase-3β, Bruton’s Tyrosine
Kinase, and Sphingosine 1 Phosphate Pathways in Multiple Sclerosis
Volume: 24
Issue: 10
Author(s): Rupali Mohite, Sankalp Gharat and Gaurav Doshi*
Affiliation:
- Department of Pharmacology, Toxicology and Therapeutics, SVKM’s Dr. Bhanuben Nanavati College of Pharmacy,
V.M. Road, Vile Parle (W), Mumbai, India
Keywords:
Autoimmune disorder, bruton’s tyrosine kinase pathway, glycogen synthase kinase-3β, multiple sclerosis, sphingosine 1-phosphate pathway, neurodegeneration.
Abstract: 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.
