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Der Forschungsschwerpunkt unserer Abteilung liegt auf der Entwicklung und Charakterisierung klinisch relevanter Tiermodelle der angeborenen Emotionalität und Stressreaktivität.
Die Arbeiten zielen auf die Analyse neurobiologischer, endokriner und molekulargenetischer Mechanismen von affektiven Störungen wie der Depression. Das Methodenspektrum umfasst eine Vielzahl verhaltensbiologischer Tests, neuroendokriner Techniken zur Analyse von Steroiden, Neuropeptiden und Transmittern im Gehirn, und darüber hinaus Paradigmen zur Untersuchung von Interaktionen zwischen genetischer Prädisposition und Umwelteinflüssen.
Die neuroendokrinen Untersuchungen im Gehirn und Blut konzentrieren sich dabei auf die Funktion und Regulation der Stresshormon-Systeme, die mit Emotionalität und Depression assoziiert sind. Zum Einsatz kommen verschiedene Labormausstämme sowie Tiermodelle für neurodegenerative Erkrankungen und affektive Störungen (generiert durch selektive Zucht bzw. gezielte genetische Manipulation).
Durch die präzise Kenntnis von neurobiologischen und molekulargenetischen Korrelaten der Verhaltensveränderungen bei Angst- und Depressionserkrankungen soll ein Beitrag zur Definition neuer Zielstrukturen für die Diagnose und Behandlung dieser affektiven Störungen geleistet werden.
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Forschungsprojekte
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.
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.
