Astrocyte Dysfunction Contributes to Post-traumatic Epilepsy
Dr. Stephanie Robel
February 1 at 12:20pm in the Fralin Auditorium, Fralin Hall room 102
Hosted by Dr. C. Finkielstein
Dr. Robel completed a Masters degree in Molecular Biology and Genetics at the Humboldt-University Berlin, Germany in 2005. During the work on her master thesis at the Max-Delbrueck Center for Molecular Medicine in Berlin she became interested in pathologies of the central nervous system. She received her Ph.D in 2010 from the Ludwig-Maximilian University in Munich, Germany, where I studied the reaction of astrocytes to brain injury. She then worked as a postdoctoral fellow at the University of Alabama at Birmingham (UAB) continuing her work on the role of astrocytes in diseases including epilepsy, glioma and trauma. Dr. Robel joined the faculty at the School of Neuroscience and the Virginia Tech Carilion research institute and as a tenure track assistant professor in the Glial Biology in Health, Disease, and Cancer Center in 2016. Her major research interest is how astrocytes shape the development and progression of neurological diseases and central nervous system trauma. Her research group is actively interrogating the molecular signature of astrogliosis and associated functional changes of astrocytes in different disease contexts by combining genetics approaches with state-of the art imaging, electrophysiology and clinically relevant models of traumatic brain injury. Her long-term goal is to molecularly dissect beneficial from detrimental aspects of astrogliosis and to identify pathways that allow therapeutic modulation of this process.
After years of assuming that neurological diseases are caused by direct damage to neurons, we now know that impaired astrocyte physiology and function precedes and is essential for the progression of many of these diseases. Focal traumatic brain injury (TBI) is a main cause of acquired epilepsies and induces scar formation, which seals focal injuries off from healthy brain tissue. This response of astrocytes comes at the cost of their homeostatic functions and it is these scars that are associated with epilepsy. Yet, the vast majority of human TBIs also presents with diffuse injury caused by acceleration-deceleration forces on the brain tissue. To determine if astrocyte scar formation is initiated and required for epileptogenesis after diffuse TBI, we modeled this injury type in mice using weight drop injury paradigm. We demonstrated that spontaneous recurrent seizures developed after a latency period. While astrocyte scar formation was absent, we identified an atypical response of astrocytes characterized by the rapid and sustained loss of homeostatic proteins and lack of astrocyte coupling. Areas with atypical astrocytes were larger in animals that later developed seizures suggesting that this response may be one root cause of epileptogenesis after diffuse TBI.
This seminar will NOT be livestreamed or recorded.