Abstract
Emerging data from experimental epilepsy models and resected human brain tissue support the proposed involvement of innate immune system activation and consequent inflammation in epilepsy. Key mediators of this process include interleukin-1β, high-mobility group box protein 1 (HMGB1), and Toll-like receptor (TLR) signaling. These recent findings constitute the basis for a novel avenue of drug development in epilepsy, one that is not only distinct from previous approaches but uniquely based on sound neurobiological evidence.
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