From October 2015 Research Associate (Akademischer Rat) and Junior Group Leader at the Institute of Pharmacy, Pharmacology, Toxicology and Clinical Pharmacy, University of Tübingen, Germany. Director: Prof. Peter Ruth.

From 2014 Brain & Behavior Research Foundation NARSAD Fellow.

2011–2013 American Heart Association Postdoctoral Fellow.

2010–2015 Postdoctoral Researcher with Prof. Johannes Hell at the Department of Pharmacology, School of Medicine, University of California Davis (UCD), Davis. Director: Prof. Donald Bers.

2006–2010 Research Assistant at the Institute of Pharmacology and Toxicology, Technische Universität München (TUM), Director: Prof. Franz Hofmann.

2006–2010 Dr. rer. nat. (Ph.D.), Institute of Pharmacology and Toxicology, TUM. Dis­sertation: “HCN2 channels in local hippocampal inhibitory interneurons constrain temporoammonic long-term potentiation”. Advisors: Prof. Harald Luksch (Chair of Zoology at TUM), Prof. Thomas Kleppisch.

2004–2006 M.Sc. in Biochemistry, TUM. Master’s thesis at the Institute of Pharmacology and Toxicology: “The role of the HCN2 channel in hippocampal synaptic plasticity”. Advisor: Prof. Thomas Kleppisch.

2001–2004 B.Sc. in Biochemistry, TUM. Bachelor’s thesis at the Institute for Clinical Chemi­stry and Pathobiochemistry, University Hospital Rechts der Isar: “Establishment of a Surface-Plasmon-Resonance Biosensor for the diagnosis of Antiphospholipid Syndrome”. Advisor: Prof. Peter B. Luppa.

1999–2001 Intermediate diploma in Chemistry, University of Zürich.

The Role of Structural Proteins in Postsynaptic Plasticity. All proteins contributing to plastic changes of synaptic transmission are part of macromolecular complexes. These involve structural proteins such as PSD-95, the major organizer of the postsynaptic site, but also components of the cytoskeleton like F-actin and α-actinin. I study the components of these complexes with the goal to elucidate how the system allows plastic changes in response to a variety of stimuli.

The components of synaptic plasticity play important roles in Excitotoxicity During Ischemic Stroke. Exhaustive overstimulation is a pathophysiological hallmark of stroke where plasticity mechanisms contribute to negative outcome. I am interested in how the postsynaptic machinery can be modified to lessen the destructive effects of excitotoxicity.

The emergence of aberrant synaptic connections during brain development is typical for Autism Spectrum Disorders (ASD). It has been shown that many proteins of the synaptic site that are important for synaptic plasticity are genetic markers associated with ASD. How do these proteins contribute to the development of functional synapses and what can be done to improve chances of regular development?