Neuroscientific and Genetic Evidence in Criminal Cases: A Double-Edged Sword in Germany but Not in the United States?

Aim of the Study: The study examines how neurobiological and genetic explanations of psychopathy influence decision-making of German law students about legal and moral responsibility and sentencing of a defendant in a case of manslaughter. Previous studies from the United States and Germany have been criticized because they partly contradict legal analyses of real-world criminal cases. With a modified design, which integrates the main criticism, we re-examined the impact of biological explanations for psychopathy on decision-making in the courtroom. Methods: We developed an improved quasi-experimental design to probe three case vignettes presenting different explanations of psychopathy in a criminal case of manslaughter. All three vignettes present the same information about a forensic expert's testimony that is said to report compelling evidence for the diagnosis of "psychopathy." The independent variable being manipulated is the type of information supporting the expert diagnosis: either no biological explanation of "psychopathy" versus a neurological explanation (brain injury) versus a genetic explanation (MAOA gene). The outcome measure is a questionnaire on legal and moral responsibility, free will, the type of custody, and the duration of the sentence. The study is adequately powered. We openly publish the data and all statistical analyses as reproducible R scripts. Results: The answers of German law students (n = 317) indicate that the omission of a neurobiological explanation is significantly associated with higher ratings of legal responsibility while compared to no biological explanation. However, there was no significant difference on the prison sentencing and type of custody assigned. Furthermore, there was no difference in the self-reported impact of the explanation of psychopathy on the participants' decision-making. Conclusion: Our findings from German law students corroborates previous research on German judges but is markedly distinct from studies on United States judges. Whereas in the United States, biological information seems to have a mitigating effect, it seems to increase the rate of involuntary commitment to forensic psychiatric hospitals in Germany

Sliding-window analysis tracks fluctuations in amygdala functional connectivity associated with physiological arousal and vigilance during fear conditioning

We evaluated whether sliding-window analysis can reveal functionally relevant brain network dynamics during a well-established fear conditioning paradigm. To this end, we tested if fMRI fluctuations in amygdala functional connectivity (FC) can be related to task-induced changes in physiological arousal and vigilance, as reflected in the skin conductance level (SCL). Thirty-two healthy individuals participated in the study. For the sliding-window analysis we used windows that were shifted by one volume at a time. Amygdala FC was calculated for each of these windows. Simultaneously acquired SCL time series were averaged over time frames that corresponded to the sliding-window FC analysis, which were subsequently associated with the whole-brain seed-based amygdala sliding-window FC using the GLM. Surrogate time series were generated to test whether connectivity dynamics could have occurred by chance. In addition, results were contrasted against static amygdala FC and sliding-window FC of the primary visual cortex, which was chosen as a control seed, while a physio-physiological interaction (PPI) was performed as cross-validation. During periods of increased SCL, the left amygdala became more strongly coupled with the bilateral insula and medial prefrontal cortex, core areas of the salience network. The sliding-window analysis yielded a connectivity pattern that was unlikely to have occurred by chance, was spatially distinct from static amygdala FC and from sliding-window FC of the primary visual cortex, but was highly comparable to that of the PPI analysis. We conclude that sliding-window analysis can reveal functionally relevant fluctuations in connectivity in the context of an externally cued task

Differences in neural recovery from acute stress between cortisol responders and non-responders

Adaptive recovery from a stressor fosters resilience. So far, however, few studies have examined brain functional connectivity in the aftermath of stress, with inconsistent results reported. Focusing on the immediate recovery from psychosocial stress, the current study compared amygdala resting-state functional connectivity (RSFC) before and immediately after psychosocial stress between cortisol responders and non-responders. Differences between groups were expected for amygdala RSFC with regions involved in down-regulation of the physiological stress response, emotion regulation, and memory consolidation. Eighty-six healthy participants (36 males/50 females) underwent a social stress paradigm inside the MRI scanner. Before and immediately after stress, resting-state (RS) fMRI scans were acquired to determine amygdala RSFC. Next, changes in connectivity from pre- to post-stress were compared between cortisol responders and non-responders. Responders demonstrated a cortisol increase, higher negative affect, and decreased heart rate variability (HRV) in response to stress compared to non-responders. A significant Sex-by-Responder-by-Time interaction was found between the bilateral amygdala and posterior cingulate cortex (PCC) and precuneus (p < 0.05, corrected). As males were also more likely to show a cortisol increase to the stress task than females, follow-up analyses were conducted for both sexes separately. Whereas no difference was observed between female responders and non-responders, male non-responders showed an increase in FC after stress between the bilateral amygdala and the PCC and precuneus (p < 0.05, corrected). The increased coupling of the amygdala with the PCC/precuneus, a core component of the default mode network (DMN), might indicate an increased engagement of the amygdala within the DMN directly after stress in non-responders. Although this study was carried out in healthy participants, and the results likely reflect normal variations in the neural response to stress, understanding the mechanisms that underlie these variations could prove beneficial in revealing neural markers that promote resilience to stress-related disorders

An fMRI Study

Individuals with borderline personality disorder (BPD) are characterized by emotional instability, impaired emotion regulation and unresolved attachment patterns associated with abusive childhood experiences. We investigated the neural response during the activation of the attachment system in BPD patients compared to healthy controls using functional magnetic resonance imaging (fMRI). Eleven female patients with BPD without posttraumatic stress disorder (PTSD) and 17 healthy female controls matched for age and education were telling stories in the scanner in response to the Adult Attachment Projective Picture System (AAP), an eight-picture set assessment of adult attachment. The picture set includes theoretically-derived attachment scenes, such as separation, death, threat and potential abuse. The picture presentation order is designed to gradually increase the activation of the attachment system. Each picture stimulus was presented for 2 min. Analyses examine group differences in attachment classifications and neural activation patterns over the course of the task. Unresolved attachment was associated with increasing amygdala activation over the course of the attachment task in patients as well as controls. Unresolved controls, but not patients, showed activation in the right dorsolateral prefrontal cortex (DLPFC) and the rostral cingulate zone (RCZ). We interpret this as a neural signature of BPD patients’ inability to exert top-down control under conditions of attachment distress. These findings point to possible neural mechanisms for underlying affective dysregulation in BPD in the context of attachment trauma and fear

A fast and intuitive method for calculating dynamic network reconfiguration and node flexibility

Dynamic interactions between brain regions, either during rest or performance of cognitive tasks, have been studied extensively using a wide variance of methods. Although some of these methods allow elegant mathematical interpretations of the data, they can easily become computationally expensive or difficult to interpret and compare between subjects or groups. Here, we propose an intuitive and computationally efficient method to measure dynamic reconfiguration of brain regions, also termed flexibility. Our flexibility measure is defined in relation to an a-priori set of biologically plausible brain modules (or networks) and does not rely on a stochastic data-driven module estimation, which, in turn, minimizes computational burden. The change of affiliation of brain regions over time with respect to these a-priori template modules is used as an indicator of brain network flexibility. We demonstrate that our proposed method yields highly similar patterns of whole-brain network reconfiguration (i.e., flexibility) during a working memory task as compared to a previous study that uses a data-driven, but computationally more expensive method. This result illustrates that the use of a fixed modular framework allows for valid, yet more efficient estimation of whole-brain flexibility, while the method additionally supports more fine-grained (e.g. node and group of nodes scale) flexibility analyses restricted to biologically plausible brain networks

Atherosclerosis and liver inflammation induced by increased dietary cholesterol intake: a combined transcriptomics and metabolomics analysis

With increasing dietary cholesterol intake the liver switches from a mainly resilient to a predominantly inflammatory state, which is associated with early lesion formation

The Temporal Dynamics of Voluntary Emotion Regulation

Background: Neuroimaging has demonstrated that voluntary emotion regulation is effective in reducing amygdala activation to aversive stimuli during regulation. However, to date little is known about the sustainability of these neural effects once active emotion regulation has been terminated. Methodology/Principal Findings: We addressed this issue by means of functional magnetic resonance imaging (fMRI) in healthy female subjects. We performed an active emotion regulation task using aversive visual scenes (task 1) and a subsequent passive viewing task using the same stimuli (task 2). Here we demonstrate not only a significantly reduced amygdala activation during active regulation but also a sustained regulation effect on the amygdala in the subsequent passive viewing task. This effect was related to an immediate increase of amygdala signal in task 1 once active emotion regulation has been terminated: The larger this peak postregulation signal in the amygdala in task 1, the smaller the sustained regulation effect in task 2. Conclusions/Significance: In summary, we found clear evidence that effects of voluntary emotion regulation extend beyond the period of active regulation. These findings are of importance for the understanding of emotion regulation i

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Genetic architecture of subcortical brain structures in 38,851 individuals

Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease