title: Does brain inflammation mediate pathological outcomes in epilepsy?
abstract: Inflammation in the central nervous system (CNS) is associated with epilepsy and is characterized by the increased levels of a complex set of soluble molecules and their receptors in epileptogenic foci with profound neuromodulatory effects. These molecules activate receptor-mediated pathways in glia and neurons that contribute to hyperexcitability in neural networks that underlie seizure generation. As a consequence, exciting new opportunities now exist for novel therapies targeting the various components of the immune system and the associated inflammatory mediators, especially the IL-1β system. This review summarizes recent findings that increased our understanding of the role of inflammation in reducing seizure threshold, contributing to seizure generation, and participating in epileptogenesis. We will discuss preclinical studies supporting the hypothesis that pharmacological inhibition of specific proinflammatory signalings may be useful to treat drug-resistant seizures in human epilepsy, and possibly delay or arrest epileptogenesis.
authors.affiliation: Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT, 84108, USA, Karen.wilcox@hsc.utah.edu.
authors.forename: Karen S
authors.initials: KS
authors.lastname: Wilcox
authors.forename: Annamaria
authors.initials: A
authors.lastname: Vezzani
mesh_terms: D004660:Encephalitis / Q000473:pathology* / Q000503:physiopathology; D004827:Epilepsy / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D009473:Neuronal Plasticity; D009435:Synaptic Transmission
chemical_list: D018836:Inflammation Mediators