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Biological Psychiatry

Projects


A02: Context effects on threat processing in dependence of testosterone levels

The focus will be on the influences of a provocative context on social threat processing in AMD under different testosterone levels. Specifically, the project aims to analyze the modulating function of context under testosterone application versus suppression on threat sensitivity in healthy controls as well as patient groups.

A04: Implicit chemosensory threat signals as stimulators of amygdala hyperresponsiveness in AMD

We make use of threat-related chemosensory stimuli, namely body odor, acquired during aggressive behavior (boxing) and unconsciously perceived, to investigate heightened amygdala responses to threat stimuli in aggressive patients. Body odors have the major advantage of being directly projected into the amygdala, circumventing cortical preprocessing, thereby enabling the differentiation of mechanisms between bottom-up altered limbic processing and top-down modulated altered cognitive evaluation.

A05: Peripersonal space violations and social threat: daily-life psychological and neural mechanisms of environmental risk for reactive aggression

Peripersonal space, the representation of the space immediately surrounding the body, will be studied as an underlying factor for threat experience. Early-life stressors and daily-life stressors will be tested as factors influencing PPS processing and associated specific brain activation patterns.

A08: The metabolic lung-brain axis in aggressive behavior in patients with AMD

Beta-hydroxy-butyrate (BHB), a ketone body, is negatively associated with aggressive behavior. BHB is a metabolite and an active signaling substrate involved in epigenetic regulation of e.g., neurotrophic factor genes in the brain.

B01: Neurobehavioral effects of repetitive prefrontal transcranial direct current stimulation (tDCS) on pathological aggression

TDCS will be used as an interventional tool to decrease aggression. Using a simultaneous tDCS – fMRI approach, the project aims to enhance cognitive control by repeated prefrontal brain stimulation, investigating its effect on aggression.

B02: Young offenders’ self-regulation deficit as a common mechanism for aggressive behavior and psychopathology - neural mechanisms and role of adverse childhood experiences

This project aims to identify cognitive and emotion control deficits in the context of negative valence and threat interference and their association with ACE in young offenders. Complementary to other projects, this project will focus on a group of young people defined by their propensity to aggression showing at the same time more severe psychopathologies.

B04: Investigating psychological and neural correlates of intimate partner violence

Focus on the neural correlates of characterizing cognitive control deficits during conflict situations. The project will investigate patients with varying levels of cognitive control along with their close partners (sibling or intimate partner) to identify the dynamics of self-regulation and co-regulation in provoked conflict situations in patients with control deficits.

C01: Gene-environment interactions and the role of impulsivity in responding to acute threats: early life stress and escalated aggression in recombinant inbred mouse strains

Sex-dependent effects and gene-environment interactions will be investigated by applying escalating aggression paradigms. Specifically, the project will investigate the effects of early life stress on aggression in response to threat and hyperactivity as well as social decision-making in 32 BXD mouse strains, the progenitor strains (C057Bl/6J and DBA/2J), and the F1 BXD cross.

C02: Aggressive decisions in social conflicts: Neuro-cognitive models for healthy individuals and psychiatric patients with high scores of aggression

Develop virtual scenarios to assess decision strategies in cartoon-like and naturalistic contexts. The core question is how healthy individuals and patients make (mal-)adaptive aggressive decisions in social conflicts given their threat sensitivity, cognitive functions, and learning experience.

C03: Distributed network control and interventions to frustrative non-reward and threat triggered aggressions

Investigate context-dependent aggression triggered by frustrative non-reward or acute social threats. Using newly developed approaches, multiple behavioral domains will be assessed in a semi-naturalistic, autonomous mouse habitat. Specifically, the habitat assesses the inter-individual dynamics of social interactions, aggressions, and hierarchy and the individual reward learning and impulsivity through different integrated modules.

C04: The sex-specific role of genes, early adversity, peers, community violence, and puberty related endocrinological changes in adolescent pathological aggression

Address sex-specific NVS (reactive aggression) and CS (different dimensions of psychopathy, proactive aggression) associated risk factors, and risk factor-based biosignatures in young people. Considering the interacting genetic, environmental, and hormonal factors related to these specific aggressive behavior dimensions, C04 will identify specific and shared factors and mechanisms related to NVS and CS in female and male youth with and without pathological aggression.

C05: The neuroanatomical underpinnings of clinical aggression and their relationship with the negative valence and cognitive control systems

Link questionnaire measures of aggression to specific neural substrates using structural MRI. The resulting patterns of aggression-related neuroanatomical variability will be co- registered with the Allen Human Brain Atlas providing gene-expression data, to highlight genes with a spatial pattern of expression that matches the neuroimaging findings.

C07: Identifying mediators of threat-aggression and experimental manipulation by tDCS

Test the interaction of the CS and frustrative non-reward as part of the NVS. It will investigate the electrophysiological correlates of frustrative feedback in aggression-prone patients. In the aftermath of induced stress, an EEG task-battery including frustrative feedback will be applied for extraction of error-related negativity (ERN) and contingent negative variation to monitor electro-physiologic signaling of the relevant learning and frustration processes.

Publications