Molecular cascades that mediate the influence of inflammation on epilepsy

Authors

  • Alon Friedman,

    1. Department of Physiology and Neurobiology, Faculty of Health Sciences, Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel
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  • Ray Dingledine

    1. Department of Pharmacology, Emory Chemical Biology Discovery Center, Emory University, Atlanta, Georgia, U.S.A.
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Address correspondence to Alon Friedman, Department of Physiology and Neurobiology, Faculty of Health Sciences. Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel. E-mail: alonf@bgu.ac.il

Summary

Experimental evidence strongly indicates a significant role for inflammatory and immune mediators in initiation of seizures and epileptogenesis. Here we will summarize data supporting the involvement of IL-1β, TNF-α and toll-like receptor 4 in seizure generation and the process of epileptogenesis. The physiological homeostasis and control over brain immune response depends on the integrity of the blood-brain barrier, transforming growth factor (TGF)-β signaling and leukocyte migration. To what extent targeting the immune system is successful in preventing epileptogenesis, and which signaling pathway should be beleaguered is still under intensive research.

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