Vascular Injury, Gliosis & Neurogenesis as Drivers for Post-Traumatic Epilepsy

Traumatic brain injury is the most common cause of acquired epilepsy. Despite our awareness that traumatic brain injury can lead to post-traumatic epilepsy, prevention of post-traumatic epilepsy with antiepileptic drugs has been unsuccessful. One reason for the lack of success may be that current treatments do not address certain potential root causes of PTE, including abnormal changes in an important type of neuronal support cell and disruption of the blood brain barrier, a barrier that blocks toxic substances from passing into the brain from the rest of the body. These changes can occur after traumatic brain injury and may increase the likelihood of seizures and post-traumatic epilepsy. Further hampering progress towards the development of treatments for post-traumatic epilepsy is a lack of adequate animal models to investigate the mechanisms behind this devastating disorder.

Dr. Harald Sontheimer and his team have identified the need for additional animal models of post-traumatic epilepsy, and plan to utilize both a new mouse model of post-traumatic epilepsy alongside an established model to investigate the ways in which traumatic brain injury leads to post-traumatic epilepsy. Their approach will focus on carefully classifying how changes that occur in the number, structure and location of neuronal support cells as well as changes in the blood brain barrier might lead to the development of post-traumatic epilepsy, with the aim of identifying new targets at which to aim treatments for post-traumatic epilepsy.