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Research Overview

Our research focuses on unravelling the function of the CD95 (Apo1/Fas)/CD95-Ligand system in the developing and diseased CNS.

In our own previous work, we showed that the death receptor CD95 is a major trigger of cell death in stroke and the injured spinal cord (Martin-Villalba et al., 1999;Martin-Villalba et al., 2001;Demjen et al., 2004). In both pre-clinical models of acute CNS trauma stimulation of CD95 leads to caspase activation and final commitment to death. In contrast, in the developing CNS, stimulation of CD95 does not result in further caspase activation and commitment to death. This is nor the case in newly generated adult neural stem cells (NSCs). Thus, by dissecting the signalling events downstream of the CD95 in developing and injured neurons we aim to ultimately design therapeutic strategies to fight neurodegeneration.

Left side: Tracing of acinar cells using Rainbow2-labeling in order to investigate homeostasis of adult pancreas, inset showing organoids resulting by proliferation of acinar cells in vitro under 3D culture conditions, formula describes the average number of nuclei in a clone, an important parameter for the mathematical modeling of acinar cell propagation. Right side: Summary of recent data related to neural stem cell (NSC) biology, bottom left shows NSCs in the center of pinwheel structures (in green) in the subventricular zone of adult mice, single-cell sequencing demonstrated heterogeneity which is illustrated by principal component analysis (PCA) in the bottom right part. These NSCs are producing newborn neurons in the olfactory bulb throughout the life of a mouse, labeled with red fluorescent protein (RFP, see top right). Interferon signaling contributes to activation of quiescent NSCs when mice are subjected to brain injury as illustrated in the upstream regulator analysis on the top left.

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