Our group is working at the cross roads of inflammation and neuronal function with molecular, cellular and behavioural approaches in various neuronal disease models. 

Molecular mechanisms involved in neuroinflammatory and neurodegenerative diseases are a result of evolutionary processes like all other biological phenomena. Therefore, understanding how these mechanisms may have evolved will eventually lead to a deeper understanding of these processes.

We investigate in depth the function of the cytokine Tumor Necrosis Factor (TNF) in neurodegenerative diseases. This pleotropic master cytokine belongs to a large family of molecules, which are able to induce apoptotic cell death but also proliferation and other cellular responses like tissue remodeling. Apoptosis plays an important role in the elimination of infected or transformed cells but also during embryonic development. TNF was found to play a major role in many neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson's disease, stroke or Multiple Sclerosis (MS), but also in depression and many other brain diseases.

In neurodegenerative diseases apoptosis seems to play a major role and therefore the pro-apoptotic function was for a long time at the center of interest to many researchers in this field. We and others have demonstrated that the TNF and the TNF receptor system is mainly a protective and sensory system guiding the tissue response to various forms of cellular stress. Apoptosis is just one of the potential responses that can be induced by TNF. We are following some of these molecular signaling mechanisms in the brain and in specific brain cells in response to TNF, and we detected various signaling molecules downstream of either TNF receptor 1 or TNF receptor 2 and their neuromodulatory signaling, e.g., glutamate receptor function, small conductance potassium channels, cAMP Epac-, PKB/Akt- signaling, Nuclear Factor kappa B or lipocalin-2 and iron metabolism.