Targeting BDNF/TrkB pathways for preventing or suppressing epilepsy.

Journal Article (Journal Article;Review)

Traumatic brain injury (TBI) and status epilepticus (SE) have both been linked to development of human epilepsy. Although distinct etiologies, current research has suggested the convergence of molecular mechanisms underlying epileptogenesis following these insults. One such mechanism involves the neurotrophin brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, tropomyosin related kinase B (TrkB). In this review, we focus on currently available data regarding the pathophysiologic role of BDNF/TrkB signaling in epilepsy development. We specifically examine the axonal injury and SE epilepsy models, two animal models that recapitulate many aspects of TBI- and SE-induced epilepsy in humans respectively. Thereafter, we discuss aspiring strategies for targeting BDNF/TrkB signaling so as to prevent epilepsy following an insult or suppress its expression once developed. This article is part of the special issue entitled 'New Epilepsy Therapies for the 21st Century - From Antiseizure Drugs to Prevention, Modification and Cure of Epilepsy'.

Full Text

Duke Authors

Cited Authors

  • Lin, TW; Harward, SC; Huang, YZ; McNamara, JO

Published Date

  • May 1, 2020

Published In

Volume / Issue

  • 167 /

Start / End Page

  • 107734 -

PubMed ID

  • 31377199

Pubmed Central ID

  • PMC7714524

Electronic International Standard Serial Number (EISSN)

  • 1873-7064

Digital Object Identifier (DOI)

  • 10.1016/j.neuropharm.2019.107734


  • eng

Conference Location

  • England