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 (Ph.D.), Neurobiology
Institute for Stem Cell Research, Helmholtz Zentrum München: Doctoral Studies (Ph.D.), Neurobiology
My 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, I have investigated the role and function of astrocytes in penetrating head injury, epilepsy, glioma and Alzheimer’s Disease. I’ve been particularly intrigued with the changes that astrocytes undergo whenever damage to the CNS occurs. This process is called astrogliosis and is surprisingly heterogeneous. Dependent on the disease context and the composition of astrocytic changes neuronal survival, health and function can be affected in beneficial or detrimental ways. My laboratory studies the process of astrogliosis in the context of repeated mild traumatic brain injury with the major goal to identify cellular mechanisms that might contribute to long-term neurodegeneration and cognitive defects in patients who incurred repeated mild TBIs.
In the US, a traumatic brain injury (TBI) occurs every 7 seconds. TBI is the major cause of long-term disability and is estimated to affect 3.2 to 5.3 million people, or approximately 1 to 2 percent of the population. About 75% 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 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.
3D reconstruction illustrating the intimate relationship between astrocytes (green) and pericytes (red) along the brain's vasculature.
See more about Robel Research Lab
- 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 drivers of abnormal neuronal activity. 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.