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Author Notes:

Corresponding authors: Eleonora Aronica MD PhD, Dept (Neuro)Pathology, Academic Medical Center, Amsterdam, The Netherlands, Phone: 31-20-5662943, Fax: 31-20-5669522, e.aronica@amc.uva.nl; Rafal M. Kaminski, UCB Pharma, Braine-l’Alleud, Belgium, Phone: 32-2-5599999, Fax: 32-2-5599900, Rafal.Kaminski@ucb.com.

Additional contributors to the studies described in this manuscript are: Valentina Iori and Teresa Ravizza (IRCCS-Mario Negri Institute for Pharmacological Research, Milano, Italy); Jackelien van Scheppingen, Cato Drion and Erwin van Vliet (Amsterdam Medical Center, Amsterdam, The Netherlands); Tobias Engel (Royal College of Surgeons in Ireland, Dublin, Ireland).

The authors declare that they have no conflict of interest to disclose.

We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.

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Research Funding:

The authors acknowledge their sources of support: Epitarget (FP7/2007-2013) under grant agreement n°602102 (AV, EA, JAG); EPISTOP (grant agreement no. 602391; EA); Epilepsiefonds “Power of the Small” and the Hersenstichting Nederland (EF-13-1; EF-14-08); Health Research Board Ireland (HRA-POR/2010/123, HRA-POR/2012/56) and Science Foundation Ireland (13/IA/1891) (to D.C.H.); AICE-FIRE and UCB Pharma Bruxelles (EP). NIH awards UO1 NS058158, R21 NS093364 and R01 NS097776 (RD).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Clinical Neurology
  • Neurosciences & Neurology
  • Inflammation
  • Immune response
  • Drug development
  • Anti-ictogenesis
  • Antiepileptogenesis
  • Disease modification
  • Epilepsy
  • TUBEROUS SCLEROSIS COMPLEX
  • FEBRILE STATUS EPILEPTICUS
  • RANDOMIZED CONTROLLED-TRIAL
  • MOBILITY GROUP BOX-1
  • TOLL-LIKE RECEPTOR
  • PROSPECTIVE COHORT
  • CYTOKINE ACTIVITY
  • CORTICAL TUBERS
  • HMGB1
  • INFLAMMATION

Neuroinflammatory targets and treatments for epilepsy validated in experimental models

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Journal Title:

Epilepsia

Volume:

Volume 58

Publisher:

, Pages 27-38

Type of Work:

Article | Post-print: After Peer Review

Abstract:

A large body of evidence that has accumulated over the past decade strongly supports the role of inflammation in the pathophysiology of human epilepsy. Specific inflammatory molecules and pathways have been identified that influence various pathologic outcomes in different experimental models of epilepsy. Most importantly, the same inflammatory pathways have also been found in surgically resected brain tissue from patients with treatment-resistant epilepsy. New antiseizure therapies may be derived from these novel potential targets. An essential and crucial question is whether targeting these molecules and pathways may result in anti-ictogenesis, antiepileptogenesis, and/or disease-modification effects. Therefore, preclinical testing in models mimicking relevant aspects of epileptogenesis is needed to guide integrated experimental and clinical trial designs. We discuss the most recent preclinical proof-of-concept studies validating a number of therapeutic approaches against inflammatory mechanisms in animal models that could represent novel avenues for drug development in epilepsy. Finally, we suggest future directions to accelerate preclinical to clinical translation of these recent discoveries.

Copyright information:

Wiley Periodicals, Inc. © 2017 International League Against Epilepsy

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