Journal article
In search of antiepileptogenic treatments for post-traumatic epilepsy
Patricia G Saletti, Idrish Ali, Pablo M Casillas-Espinosa, Bridgette D Semple, Christos Panagiotis Lisgaras, Solomon L Moshe, Aristea S Galanopoulou
NEUROBIOLOGY OF DISEASE | ACADEMIC PRESS INC ELSEVIER SCIENCE | Published : 2019
Abstract
Post-traumatic epilepsy (PTE) is diagnosed in 20% of individuals with acquired epilepsy, and can impact significantly the quality of life due to the seizures and other functional or cognitive and behavioral outcomes of the traumatic brain injury (TBI) and PTE. There is no available antiepileptogenic or disease modifying treatment for PTE. Animal models of TBI and PTE have been developed, offering useful insights on the value of inflammatory, neurodegenerative pathways, hemorrhages and iron accumulation, calcium channels and other target pathways that could be used for treatment development. Most of the existing preclinical studies test efficacy towards pathologies of functional recovery afte..
View full abstractGrants
Awarded by NIHU54
Awarded by US Department of Defense
Awarded by NINDSRO1
Awarded by NINDS Center without Walls
Awarded by United States Department of Defense
Funding Acknowledgements
PS and CL have no conflicts of interest in regards to this manuscript. IA has funding support from the Melbourne University Early Career Research grant. IA has no conflicts of interest in regards to the contents of this manuscript. PMCE acknowledges support from the Melbourne University Early Career Research grant. PMCE has no conflicts of interest in regards to the contents of this manuscript. BDS acknowledges support from the National Health and Medical Research Council of Australia (NHMRC) and Monash University. BDS has no conflicts of interest in regards to the contents of this manuscript. SLM is the Charles Frost Chair in Neurosurgery and Neurology and partially funded by grants from NIHU54 NS100064 and NS43209, US Department of Defense (W81XWH-13-1-0180), and the Heifer Family and the Segal Family Foundations and the Abbe Goldstein/Joshua Lurie and Laurie Marsh/Dan Levitz families. S.L.M. has no conflicts of interest in regards to this article. He is serving as Associate Editor of Neurobiology of Disease and is on the editorial board of Brain and Development, Pediatric Neurology and Physiological Research. He receives from Elsevier an annual compensation for his work as Associate Editor in Neurobiology of Disease and royalties from 2 books he co-edited. He received a consultant fee from UCB for participation in a DSMB. He has also received honorarium for participation in an advisory board meeting of Mallinckrodt, but there is no conflict of interest in regards to the contents of this manuscript. ASG acknowledges grant support by NINDSRO1 NS091170, the NINDS Center without WallsU54 NS100064 (EpiBioS4Rx), the United States Department of Defense (W81XWH-13-1-0180), research funding from the Heifer Family, the Segal Family Foundations and the Abbe Goldstein/Joshua Lurie and Laurie Marsh/Dan Levitz families. ASG has received royalties for publications from Elsevier and a one-time honorarium for participation at a scientific advisory board for Mallinckrodt and is a co-Editor-in-Chief at Epilepsia Open but has no conflicts in regards to this article.