Research projects

The focus of our research group is to generate and characterize clinically relevant animal models of inborn (trait) emotionality and stress reactivity.

We aim to elucidate neurobiological, endocrine and molecular-genetic mechanisms underlying behavioural, physiological and neurobiological changes in affective disorders such as major depression. It is only with deep insight into these mechanisms that novel treatment strategies and promising targets for therapeutic interventions can be developed in the future. Such in-depth understanding is ultimately essential to realizing our goal of predictive, preventive and personalized medicine.

The spectrum of our research includes projects at the genetic, proteomic and systemic level. We apply a wide variety of behavioural tests assessing emotionality, stress-coping and cognitive functions along with neuroendocrine approaches to analyze neuropeptides and proteins involved in the activity and regulation of the hypothalamic-pituitary-adrenocortical (HPA) axis. Furthermore, we use paradigms addressing the interaction between genetic predispositions and environmental influences such as exposure to early life stress, shedding light on the epigenetic modification of gene expression, behavioural traits and neurobiological endophenotypes.



Genetic risk factors and early life stress interact to shape endophenotypes of affective disorders: neuroendocrine, cognitive and behavioural effects of this G x E interaction

Epidemiological studies have proven a strong impact of an individual’s genetic constitution on traits linked with affective disorders such as major depression. Through large scale genomic screening studies, certain genes or alleles have been associated with an increased risk of developing these disorders. However, genes never act in isolation but are embedded in organisms that develop and live in a complex environment.

Stress responsiveness and cognition: revealing the impact of a genetic predisposition to increased HPA axis reactivity on learning and memory

Cognitive deficits in depressed patients have recently received increasing attention. These symptoms are mainly in the realm of executive functioning deficits and include hippocampus-dependent and prefrontal cortex (PFC)-dependent tasks. The stress reactivity (SR) mouse model is of potential interest in modeling these deficits as glucocorticoid exposure has detrimental effects on both the hippocampus and PFC as these brain regions express abundant amounts of glucocorticoid receptors.

Identification of novel genomic loci contributing to affective disorders

Complex multidimensional diseases such as major depression are determined by a variety of genetic and environmental factors, each of them ultimately contributing with minor effect size to the characteristic endophenotypes and the aetiology of the disease. The identification of genetic loci involved has therefore turned out to be complicated and was accompanied by setbacks.

Altered hippocampal energy metabolism in a mouse model of affective disorders: Insights from transcriptomic, proteomic and neurophysiological approaches

Gene and protein expression profiling experiments as well as neurophysiological assessments were conducted aiming to elucidate the relevance of differentially expressed genes, proteins and brain activity for the endophenotypes of the stress reactivity (SR) mouse model of affective disorders (HR/IR/LR lines).

Endophenotyping of mice selected for extremes in stress reactivity: the HR/IR/LR mouse model of affective disorders

Dysfunctions of the hypothalamic-pituitary-adrenal (HPA) axis are closely associated with the pathophysiology of affective disorders such as major depression (MD). Accordingly, patients suffering from MD frequently show profound neuroendocrine alterations with hyper- or hypo-cortisolism as a result of a dysregulated stress hormone system.