Bidirectional Mechanism Of Neuroinflammation And Drug-Resistant Epilepsy

Abstract

The intricate process of neuroinflammation begins with the activation of glial cells and continues with the production of chemokines and cytokines that promote inflammation. Evidence suggests that neuroinflammation is prevalent in epileptic humans and animal models alike. There is a complex two-way street between neuroinflammation and drug-resistant epilepsy (DRE). On one hand, neuroinflammation helps build and sustain DRE, and on the other hand, seizures can cause neuroinflammation, which in turn causes more seizures. Many theories have been put up to clarify the connection between neuroinflammation and DRE, such as the involvement of Toll-like receptors, the NF-κB pathway, and the activation of ALK-5. Several anti-inflammatory drugs have shown benefit in animal models of epilepsy, suggesting that targeting neuroinflammation might be a potential strategy for the treatment of DRE. Nevertheless, more studies are required to ascertain the effectiveness and safety of these medicines when administered to human patients suffering from DRE. Novel treatments for this illness may be developed by understanding the processes behind the bidirectional link between neuroinflammation and DRE.