Dr. Gabor Petzold

Biography

Gabor Petzold studied medicine in Germany, Hungary, the USA and UK, and completed his MD thesis at the Department of Neurology at Düsseldorf University, Germany. From 2000 to 2005, he was a postdoctoral fellow at the Department of Experimental Neurology (Head: U. Dirnagl) as well as a resident in Neurology at the Department of Neurology (Head: K. M. Einhäupl) at Charité Medical School, Berlin, Germany. From 2005 to 2008, he was a research fellow of the German Science Foundation (DFG) and a Marie Curie Fellow of the European Union at V. N. Murthy’s laboratory at the Center for Brain Science (Harvard University). in 2008 he became group leader at the Department of Experimental Neurology, Charité Berlin. He completed his board certification in Neurology, and received his “Habilitation” in 2009. In 2009, he received the Young Scientist Award from the German Stroke Competence Network. From 2009 to 2010, he worked as a clinical consultant/attending in Neurology at the Charité. He joined the DZNE in 2011 as group leader of the Neurovascular Diseases Research Group and coordinator of vascular dementia research at the DZNE Bonn site. In addition, he is a clinical consultant/attending in Neurology, and supervises the vascular outpatient department, as well as the clinical Stroke Unit (together with U. Wüllner) , at the Department of Neurology (Head: T. Klockgether) at the University Hospital Bonn.

Research Interest

Changes in cerebral blood flow (CBF) are centrally involved in the pathogenesis of neurological diseases. A prominent example is stroke (cerebral ischemia), in which blood flow to a brain region is acutely reduced or completely blocked. Moreover, a milder but chronic reduction in CBF can lead to cognitive impairment and vascular dementia, i. e. the second most common form of dementia after Alzheimer’s disease. Despite its prevalence and socioeconomic impact, the pathogenesis and therapeutic options of vascular dementia have remained largely unexplored. In addition to these primarily vascular disorders, it has become increasingly apparent in recent years that profound changes in CBF also occur in many neurodegenerative disorders. For example, cardiovascular diseases such as hypertension and dyslipidemia are important risk factors for the development of Alzheimer’s disease. Moreover, CBF dysregulation occurs very early in many neurodegenerative diseases, indicating that the disruption of CBF may constitute an initial and common step in the pathogenesis of these disorders, and that augmentation of CBF may prove therapeutically beneficial. We aim to identify the cellular signaling pathways and mechanisms responsible for the changes in CBF regulation in acute neurological and neurodegenerative diseases. In addition, we seek to investigate how neurodegeneration may increase the brain’s vulnerability for CBF disruption. We are particularly interested in the role of astrocytes. These glial cells are involved in the pathogenesis in many neurodegenerative disorders (e. g. Alzheimer’s disease, stroke, amytrophic lateral sclerosis). Moreover, we have recently shown that they are central regulators of CBF under physiological conditions, indicating that a perturbation of astrocytic pathways may underlie vascular dysregulation in neurological diseases. We investigate these questions in animal models of Alzheimer’s disease, vascular dementia, stroke, and diabetes, using techniques such as in vivo two-photon microscopy, MRI, electropyhsiology, genetic and pharmacological calcium indicators, and behavioral tests. In addition, we seek to translate our experimental findings into clinical studies. To this end, we are involved in the conception and execution of a number of clinical studies investigating therapeutic strategies in stroke, as well as the mechanisms of vascular cognitive impairment.