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Stroke Research

Group Leader: Dominik Michailski (Department of Neurology)

Group Members: Wolfgang Härtig | Martin Krüger | Bianca Mages | Susanne Aleithe | Alexandra Blietz | Stephan Altmann


Ischemic stroke represents one of the leading causes of death worldwide with mortality rates of up to 30% within the 12 months. Unfortunately, available causal treatment strategies to restore cerebral blood flow are still limited to a rather short time window of a few hours after ischemia onset and are thus available to a minority of the patients concerned. Using models of experimental focal cerebral ischemia, the group characterizes the process of transition from a transient towards long lasting tissue damage after stroke. In this context, the group analyzes intra- and extracellular structure stabilizing elements in the setting of ischemia and reperfusion at different time points after ischemia onset. In close collaboration with clinical and preclinical departments of the University of Leipzig, this group is thus aiming at the identification and development of novel complementary treatment strategies. (funded by Europäischer Sozialfonds)


Data

Martin Krüger

Email : martin.krueger@medizin.uni-leipzig.de

Phone : +49 341 9722073

Address : Institute of Anatomy | Eilenburger Str. 13-15 | D-04317 Leipzig


Project

Characterization of vascular affection and blood-brain barrier breakdown following focal cerebral ischemia

Martin Krüger

funded by (Europäischer Sozialfonds)

In the setting of stroke, ischemia clinically not only affects the neuronal function of patients concerned, but also the function of the cerebral vasculature. Here, a loss of the blood-brain barrier (BBB) function of affected vessels contributes to an ischemia-related brain edema, which critically impacts on the clinical outcome. In this context, we are aiming to characterize the patterns of ischemia-related BBB breakdown using different and translationally relevant models of experimentally induced focal cerebral ischemia and reperfusion at different time points after ischemia induction. Thereby we are able to determine the time course and the extent of the associated BBB breakdown in vessels showing an increased permeability using light-, fluorescence- and electron microscopy. In this context, we were able to demonstrate severe degenerations in vessels showing loss of BBB integrity, which not only involve the endothelial layer, but also the vascular wall. Of note, distinct stages of vascular affection were identified in different sections of the vascular tree, which can be used to evaluate and compare the integrity of the cerebral vasculature at different time points and in different regions of the affected brain parenchyma. Further, our data highlights the significance of the endothelial and vascular integrity for the development of an ischemia-related brain edema. Thus, protection of endothelial cells is likely to represent a promising target for additional neuroprotective strategies.