About

The group focuses on the very interface between bed-side clinical neurology and experimental models and rapid transport of basic ideas and application into preclinical testing.

The major targets include signaling mechanisms of inflammation and proteolytic vascular damage underlying thromboembolism as well as hemorrhage formation with and without thrombolytic therapy.

The main research lines:

• the progression of acute ischemic neuronal injury, activation of inflammatory cells, BBB damage and hemorrhage formation in the brain parenchyma
• translation of basic science knowledge into clinical therapy of stroke – practical implementation of ‘time is brain’
• rodent models of cerebral ischemia
• human brain bank of infarcted brain tissue
• the etiologic mechanisms by which asymptomatic carotid artery disease is transformed into a symtomatic one to cause strokes.
• human carotid artery samples from a large number of individuals with symptomatic or asymptomatic disease
• blood and DNA samples together with ample clinical and imaging data from the same subjects
• ultra-acute biomarkers of BBB breakdown in acute stroke
• basilar occlusion as the most devastating form of clinical stroke

Within these research lines we have established reproducible animal models in acute cerebral ischemia and hemorrhage and applied several imaging, tracing, histopathological and immunohistochemical techniques to monitor brain damage. We also utilize DNA-microarray technology to and have performed global genomic analyses from the human tissue materials.

We welcome new ambitious investigators (PhD or MD) with some experience in the above methodologies to join our group and excel in basic, yet clinically oriented neuroscience.