Cellular and Molecular Mechanisms of Neuroinflammation in Epilepsy
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abstract
Epilepsy affects millions of people worldwide. Epilepsy is a chronic neurological disorder characterized by recurrent unprovoked seizures. Neuronal damage and inflammation are suggested to play a central role in the pathophysiology of epileptogenesis and chronic epilepsy. There is increasing evidence that excessive inflammatory actions of the neuroimmune system may contribute to the development of epilepsy following a variety of precipitating conditions, including brain injury, prolonged seizure events or status epilepticus, brain infections, stroke, and neurotoxicity. This review describes the current status of neuroinflammation in epilepsy and the therapeutic promise of targeting the brain immune system for chronic blockade of inflammation as an effective approach for preventing the onset of epilepsy and related hyperexcitability conditions. The inflammatory reaction is mediated by microglia, astrocytes, and other brain immune cells. It is well established that proinflammatory cytokines, interleukins, and related factors are critically involved in processes linked to epileptogenesis. Consequently, a variety of targeted therapeutic approaches have been tested in experimental models of epilepsy. There are many promising pharmacological strategies for targeted modulation of neuroinflammation including microglia inhibitors, cyclooxygenase inhibitors, prostaglandin receptor antagonists, and interleukin inhibitors. Overall, current reports suggest that many key outcome parameters of hyperexcitability, epileptogenesis, and neuroprotection have been successfully inhibited by specific blockade of proinflammatory signaling in the brain
