How does the kidney signal to the brain?
How do microglia cells and neurons communicate?
How does cognitive decline occur?
Who "talks" to whom?
These are only some of the questions we want to answer.
Inflammation within the central nervous system has a variety of causalities. We aim to decipher the role of coagulation proteases in the context of cognitive decline. Coagulation proteases may play a pivotal role in the maintenance of signaling processes and ion homeostasis in certain pathologies. The activity of activated Protein C is influenced in various diseases, such as kidney disease, thereby leading to potentially altered signaling processes in the brain.
In our group we furthermore investigate how and to what extend the brain homeostasis is influenced in a mouse model of chronic kidney disease. In this context we study the cell-cell communication between microglia and neurons. One of our goals is to analyze the blood brain barrier composition and its impairment in disorders with cognitive decline.
In order to realize our ideas, we apply a variety of in vitro approaches (cell culture, lentiviral induced knock-down, CRISPR-Cas9 mediated knock-out, co-cultures, migration assays) as well as in vivo studies using different genotypes (Cre-mediated cell specific knock-out, inducible mutations).
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