Format

Send to

Choose Destination
Adv Exp Med Biol. 2014;813:169-83. doi: 10.1007/978-94-017-8914-1_14.

Does brain inflammation mediate pathological outcomes in epilepsy?

Author information

1
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT, 84108, USA, Karen.wilcox@hsc.utah.edu.

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.

PMID:
25012376
PMCID:
PMC4867105
DOI:
10.1007/978-94-017-8914-1_14
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Springer Icon for PubMed Central
Loading ...
Support Center