Stefanie Robel, Ph.D.
Assistant Professor, Virginia Tech Carilion Research Institute
Assistant Professor, School of Neuroscience, College of Science, Virginia Tech
Dr. Robel’s research interest is in the role of astrocytes, star-shaped glial cells, in the development and progression of CNS diseases. As a doctoral student in the laboratory of Dr. Magdalena Götz in Munich, Germany, and as a postdoctoral fellow in Dr. Harald Sontheimer’s laboratory at the University of Alabama at Birmingham, Dr. Robel has investigated the role and function of astrocytes in penetrating head injury, epilepsy, glioma and Alzheimer’s Disease. In keeping with this theme, Dr. Robel’s independent line of research seeks to elucidate the role of astrocytes after repeated mild traumatic brain injury.
In the US, a traumatic brain injury (TBI) occurs every seven seconds. TBI is the major cause of long-term disability and is estimated to affect 3.2 to 5.3 million people, or approximately one to two percent of the population. About 75 percent of these injuries are classified as mild TBI or concussion, which by definition presents without tissue damage in standard CT imaging. In addition to the immediate and/or lifelong consequences for cognitive function, patients who experienced a TBI have an increased risk for the development of neurodegenerative diseases later in life. This has undergone increased scrutiny recently in athletes and military personnel who have suffered repeated injuries. The cause for the pronounced neuronal cell death decades after the initial injuries occurred, has remained a mystery. However, improved imaging techniques have revealed microbleeds in a majority of these patients indicative of blood-brain barrier damage. Mild TBI is also associated with reduced cerebral blood flow in patients. Since the brain is critically dependent on a sustained blood flow, its reduction after TBI might initiate a cascade of detrimental events that can lead to slowly progressing tissue damage.
Sufficient blood supply of active brain regions and the immune-privileged status of the CNS are assured by the neurovascular unit, a functional entity consisting of neural and vascular cells. Astrocytes are part of the neurovascular unit modulating the regulation of blood flow and likely contributing to blood-brain barrier integrity and maintenance. Yet, little is known about the astrocyte-vascular interface and its functionality in the context of CNS disease. To study the role of astrocytes in CNS pathology after repeated mild TBI, we use state-of-the-art models of TBI in transgenic mice in combination with confocal and in vivo 2-photon imaging.
For a full listing of Dr. Robel's publications, visit PubMed.
Education and Training
- Potsdam University: Bachelor of Science, Biology
- Humboldt University: Master of Science, Biology, Molecular Biology and Genetics
- Max Delbrück Center for Molecular Medicine: Master's Thesis, Molecular Medicine
- Institute for Physiological Genomics, Ludwigs-Maximilians University: Doctoral Studies (PhD), Neurobiology
- Institute for Stem Cell Research, Helmholtz Zentrum München: Doctoral Studies (PhD), Neurobiology
- University of Alabama at Birmingham
Instructor, Department of Neurobiology
Postdoctoral Fellow, Department of Neurobiology
- Ludwigs-Maximilians University, Institute for Physiological Genomics
Awards and Honors
- Chair, Executive Board UAB Postdoctoral Association, June 2014-May 2015
- Head of Laboratory during Dr. Sontheimer's sabbatical leave, January-May 2014
- Research Award of $10,000, Alzheimer's of Central Alabama, 2013
- Research Fellowship of $100,000 for two years, American Brain Tumor Association, 2013
- Research Fellowship of $45,000, Epilepsy Foundation, 2012
- Emerging Scholar Award, Civitan International Research Center, 2011
- Postdoctoral Scholar Award, University of Alabama at Birmingham, 2011
- Research Fellowship, German Research Council, 2011
- GLIA Travel Stipend, 2009
- Robel S, Buckingham SC, Boni JL, Campbell SL, Danbolt NC, Riedmann T, Sutor B, Sontheimer H. (2015). Reactive astrogliosis causes the development of spontaneous seizures. Journal of Neuroscience 35(8): 3330-45.
- Robel S, Sontheimer H. (2015). Glia as active players in acquired epilepsy. Nature Neuroscience.
- Kimbrough IF*, Robel S*, Roberson E, Sontheimer H. (2015). Vascular amyloidosis impairs the gliovascular unit in the hAPPJ20 mouse model of Alzheimer disease. BRAIN.
- Watkins S, Robel S, Kimbrough IK, Robert SM, Ellis-Davies G, Sontheimer H. (2014). Disruption of astrocyte-vascular coupling and the blood-brain barrier by invading glioma cells. Nature Communications 5.
- Buckingham SC, Robel S. (2013). Glutamate and tumor-associated epilepsy: glial cell dysfunction in the peritumoral environment. Neurochemistry International 63(7).
- Robel S, Baradehle S, Lepier A, Brakebusch C, Gotz M. (2011). Genetic deletion of Cdc42 reveals a crucial role for astrocyte recruitment to the injury site in vitro and in vivo. Journal of Neuroscience 31(35): 12471-82.
- Robel S, Berninger B, Gotz M. (2011). The stem cell potential of glia: lessons from reactive gliosis. Nature Reviews Neuroscience 12(2): 88-104.
- Robel S, Tetsuji M, Zoubaa S, Schlegel J, Sirko S, Faissner A, Goebbels S, Dimou L, Gotz M. (2009). Conditional deletion of β1-Integrin in astroglia causes partial reactive gliosis. GLIA 57(15): 1630-47.