Andreas Heinz

Humboldt-Universität zu Berlin, Berlín, Berlin, Germany

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Publications (748)2954.7 Total impact

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    ABSTRACT: In alcohol dependence, individual prediction of treatment outcome based on neuroimaging endophenotypes can help to tailor individual therapeutic offers to patients depending on their relapse risk. We built a prediction model for prospective relapse of alcohol-dependent patients that combines structural and functional brain images derived from an experiment in which 46 subjects were exposed to alcohol-related cues. The patient group had been subdivided post hoc regarding relapse behavior defined as a consumption of more than 60 g alcohol for male or more than 40 g alcohol for female patients on one occasion during the 3-month assessment period (16 abstainers and 30 relapsers). Naïve Bayes, support vector machines and learning vector quantization were used to infer prediction models for relapse based on the mean and maximum values of gray matter volume and brain responses on alcohol-related cues within a priori defined regions of interest. Model performance was estimated by leave-one-out cross-validation. Learning vector quantization yielded the model with the highest balanced accuracy (79.4 percent, p < 0.0001; 90 percent sensitivity, 68.8 percent specificity). The most informative individual predictors were functional brain activation features in the right and left ventral tegmental areas and the right ventral striatum, as well as gray matter volume features in left orbitofrontal cortex and right medial prefrontal cortex. In contrast, the best pure clinical model reached only chance-level accuracy (61.3 percent). Our results indicate that an individual prediction of future relapse from imaging measurement outperforms prediction from clinical measurements. The approach may help to target specific interventions at different risk groups.
    Addiction Biology 10/2015; DOI:10.1111/adb.12302 · 5.36 Impact Factor
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    ABSTRACT: Gaze direction and especially direct gaze is a powerful nonverbal cue that plays an important role in social interactions. Here we studied the neural mechanisms underlying the privileged access of direct gaze to visual awareness. We performed functional magnetic resonance imaging in healthy human volunteers who were exposed to faces with direct or averted gaze under continuous flash suppression, thereby manipulating their awareness of the faces. A gaze processing network comprising fusiform face area (FFA), superior temporal sulcus, amygdala, and intraparietal sulcus showed overall reduced neural responses when participants reported to be unaware of the faces. Interestingly, direct gaze elicited greater responses than averted gaze when participants were aware of the faces, but smaller responses when they were unaware. Additional between-subject correlation and single-trial analyses indicated that this pattern of results was due to a modulation of the relationship between neural responses and awareness by gaze direction: with increasing neural activation in the FFA, direct-gaze faces entered awareness more readily than averted-gaze faces. These findings suggest that for direct gaze, lower levels of neural activity are sufficient to give rise to awareness than for averted gaze, thus providing a neural basis for privileged access of direct gaze to awareness.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 09/2015; 35(39):13287-13299. DOI:10.1523/JNEUROSCI.0815-15.2015 · 6.34 Impact Factor
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    ABSTRACT: Cannabis use in adolescence may be characterized by differences in the neural basis of affective processing. In this study, we used an fMRI affective face processing task to compare a large group (n = 70) of 14-year olds with a history of cannabis use to a group (n = 70) of never-using controls matched on numerous characteristics including IQ, SES, alcohol and cigarette use. The task contained short movies displaying angry and neutral faces. Results indicated cannabis users had greater reactivity in the bilateral amygdalae to angry faces than neutral faces, an effect that was not observed in their abstinent peers. In contrast, activity levels in the cannabis users in cortical areas including the right temporal-parietal junction and bilateral dorsolateral prefrontal cortex did not discriminate between the two face conditions, but did differ in controls. Results did not change after excluding subjects with any psychiatric symptomology. Given the high density of cannabinoid receptors in the amygdala, our findings suggest cannabis use in early adolescence is associated with hypersensitivity to signals of threat. Hypersensitivity to negative affect in adolescence may place the subject at-risk for mood disorders in adulthood.
    Developmental Cognitive Neuroscience 09/2015; DOI:10.1016/j.dcn.2015.08.007 · 3.83 Impact Factor
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    ABSTRACT: As evidenced by a multitude of studies, abnormalities in Theory of Mind (ToM) and its neural processing might constitute an intermediate phenotype of schizophrenia. If so, neural alterations during ToM should be observable in unaffected relatives of patients as well, since they share a considerable amount of genetic risk. While behaviorally, impaired ToM function is confirmed meta-analytically in relatives, evidence on aberrant function of the neural ToM network is sparse and inconclusive. The present study therefore aimed to further explore the neural correlates of ToM in relatives of schizophrenia. 297 controls and 63 unaffected first-degree relatives of patients with schizophrenia performed a ToM task during functional magnetic resonance imaging. Consistent with the literature relatives exhibited decreased activity of the medial prefrontal cortex. Additionally, increased recruitment of the right middle temporal gyrus and posterior cingulate cortex was found, which was related to subclinical paranoid symptoms in relatives. These results further support decreased medial prefrontal activation during ToM as an intermediate phenotype of genetic risk for schizophrenia. Enhanced recruitment of posterior ToM areas in relatives might indicate inefficiency mechanisms in the presence of genetic risk. © The Author (2015). Published by Oxford University Press. For Permissions, please email:
    Social Cognitive and Affective Neuroscience 09/2015; DOI:10.1093/scan/nsv111 · 7.37 Impact Factor
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    ABSTRACT: The brain is an inherently dynamic system, and executive cognition requires dynamically reconfiguring, highly evolving networks of brain regions that interact in complex and transient communication patterns. However, a precise characterization of these reconfiguration processes during cognitive function in humans remains elusive. Here, we use a series of techniques developed in the field of "dynamic network neuroscience" to investigate the dynamics of functional brain networks in 344 healthy subjects during a working-memory challenge (the "n-back" task). In contrast to a control condition, in which dynamic changes in cortical networks were spread evenly across systems, the effortful working-memory condition was characterized by a reconfiguration of frontoparietal and frontotemporal networks. This reconfiguration, which characterizes "network flexibility," employs transient and heterogeneous connectivity between frontal systems, which we refer to as "integration." Frontal integration predicted neuropsychological measures requiring working memory and executive cognition, suggesting that dynamic network reconfiguration between frontal systems supports those functions. Our results characterize dynamic reconfiguration of large-scale distributed neural circuits during executive cognition in humans and have implications for understanding impaired cognitive function in disorders affecting connectivity, such as schizophrenia or dementia.
    Proceedings of the National Academy of Sciences 08/2015; DOI:10.1073/pnas.1422487112 · 9.67 Impact Factor
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    ABSTRACT: Cannabis use during adolescence is known to increase the risk for schizophrenia in men. Sex differences in the dynamics of brain maturation during adolescence may be of particular importance with regard to vulnerability of the male brain to cannabis exposure. To evaluate whether the association between cannabis use and cortical maturation in adolescents is moderated by a polygenic risk score for schizophrenia. Observation of 3 population-based samples included initial analysis in 1024 adolescents of both sexes from the Canadian Saguenay Youth Study (SYS) and follow-up in 426 adolescents of both sexes from the IMAGEN Study from 8 European cities and 504 male youth from the Avon Longitudinal Study of Parents and Children (ALSPAC) based in England. A total of 1577 participants (aged 12-21 years; 899 [57.0%] male) had (1) information about cannabis use; (2) imaging studies of the brain; and (3) a polygenic risk score for schizophrenia across 108 genetic loci identified by the Psychiatric Genomics Consortium. Data analysis was performed from March 1 through December 31, 2014. Cortical thickness derived from T1-weighted magnetic resonance images. Linear regression tests were used to assess the relationships between cannabis use, cortical thickness, and risk score. Across the 3 samples of 1574 participants, a negative association was observed between cannabis use in early adolescence and cortical thickness in male participants with a high polygenic risk score. This observation was not the case for low-risk male participants or for the low- or high-risk female participants. Thus, in SYS male participants, cannabis use interacted with risk score vis-à-vis cortical thickness (P = .009); higher scores were associated with lower thickness only in males who used cannabis. Similarly, in the IMAGEN male participants, cannabis use interacted with increased risk score vis-à-vis a change in decreasing cortical thickness from 14.5 to 18.5 years of age (t137 = -2.36; P = .02). Finally, in the ALSPAC high-risk group of male participants, those who used cannabis most frequently (≥61 occasions) had lower cortical thickness than those who never used cannabis (difference in cortical thickness, 0.07 [95% CI, 0.01-0.12]; P = .02) and those with light use (<5 occasions) (difference in cortical thickness, 0.11 [95% CI, 0.03-0.18]; P = .004). Cannabis use in early adolescence moderates the association between the genetic risk for schizophrenia and cortical maturation among male individuals. This finding implicates processes underlying cortical maturation in mediating the link between cannabis use and liability to schizophrenia.
    JAMA Psychiatry 08/2015; DOI:10.1001/jamapsychiatry.2015.1131 · 12.01 Impact Factor
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    ABSTRACT: The aim of the current study was to determine genotype effects of four single nucleotide polymorphisms (SNPs) in the genes of the N-Methyl-d-aspartate receptor (GRIN1, GRIN2A, GRIN2C) and kainate receptor (GRIK1), which have been previously associated with alcoholism, on behavior, neural cue-reactivity and drinking outcome. Eighty-six abstinent alcohol dependent patients were recruited from an in-patient setting. Neuropsychological tests, genotyping and functional magnetic resonance imaging (fMRI) were used to study genotype effects. GRIN2C risk allele carriers displayed increased alcohol cue-induced activation in the anterior cingulate cortex (ACC) and dorsolateral prefrontal cortex (dlPFC). Neural activation in the ACC positively correlated with craving for alcohol (r = 0.201, P = 0.032), whereas activation in the dlPFC showed a negative association (r = -0.215, P = 0.023). In addition, dlPFC activation predicted time to first relapse (HR = 2.701, 95%CI 1.244-5.864, P = 0.012). GRIK1 risk allele carriers showed increased cue-induced activation in the medial prefrontal (PFC) and orbitofrontal cortex (OFC) and in the lateral PFC and OFC. Activation in both clusters positively correlated with alcohol craving (rmedOFC, medPFC = 0.403, P = 0.001, rlatOFC, latPFC = 0.282, P = 0.008), and activation in the cluster that encompassed the medial OFC predicted time to first relapse (HR = 1.911, 95%CI 1.030-3.545, P = 0.040). Findings indicate that SNPs in the GRIN2C and GRIK1 genes are associated with altered cue-induced brain activation that is related to craving for alcohol and relapse risk. © 2015 Society for the Study of Addiction.
    Addiction Biology 08/2015; DOI:10.1111/adb.12291 · 5.36 Impact Factor
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    ABSTRACT: Discrimination is linked to various health problems, including mental disorders like depression and also has a negative effect on the access to mental health care services. Little is known about factors mitigating the association between ethnic discrimination and mental distress. The present study examined the extent of the relationship between perceived ethnic discrimination and psychological distress among women of Turkish origin residing in Berlin, and explored whether this association is moderated by acculturation strategies while controlling for known predictors of distress in migrant populations. A total of 205 women of Turkish origin participated in the study. 55.1 % of the participants reported some degree of ethnic discrimination. The degree of reported discrimination varied according to acculturation. The highest level of ethnic discrimination was found in the second generation separated group and both generations of the marginalized group. Further, the results indicate an association between ethnic discrimination and distress while adjusting for known socio-demographic predictors of distress, migration-related factors, and neuroticism (B = 5.56, 95 % CI 2.44-8.68, p < 0.001). However, the relationship did vary as a function of acculturation strategy, showing an association only in the separated group. The findings highlight the effects of ethnic discrimination beyond the influence of known risk factor for psychological distress in migrants, such as unemployment, being single, having a limited residence permit or the presence of personality structures that may increase vulnerability for stress responses and mental disorders.
    Social Psychiatry 08/2015; DOI:10.1007/s00127-015-1105-3 · 2.54 Impact Factor
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    ABSTRACT: A dysfunctional differentiation between self-relevant and irrelevant information may affect the perception of environmental stimuli as abnormally salient. The aberrant salience hypothesis assumes that positive symptoms arise from an attribution of salience to irrelevant stimuli accompanied by the feeling of self-relevance. Self-referential processing relies on the activation of cortical midline structures which was demonstrated to be impaired in psychosis. We investigated the neural correlates of self-referential processing, aberrant salience attribution, and the relationship between these 2 measures across the psychosis continuum. Twenty-nine schizophrenia patients, 24 healthy individuals with subclinical delusional ideation, and 50 healthy individuals participated in this study. Aberrant salience was assessed behaviorally in terms of reaction times to task irrelevant cues. Participants performed a self-reference task during fMRI in which they had to apply neutral trait words to them or to a public figure. The correlation between self-referential processing and aberrant salience attribution was tested. Schizophrenia patients displayed increased aberrant salience attribution compared with healthy controls and individuals with subclinical delusional ideation, while the latter exhibited intermediate aberrant salience scores. In the self-reference task, schizophrenia patients showed reduced activation in the ventromedial prefrontal cortex (vmPFC), but individuals with subclinical delusional ideation did not differ from healthy controls. In schizophrenia patients, vmPFC activation correlated negatively with implicit aberrant salience attribution. Higher aberrant salience attribution in schizophrenia patients is related to reduced vmPFC activation during self-referential judgments suggesting that aberrant relevance coding is reflected in decreased neural self-referential processing as well as in aberrant salience attribution. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email:
    Schizophrenia Bulletin 07/2015; DOI:10.1093/schbul/sbv098 · 8.45 Impact Factor
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    ABSTRACT: The striatum is known to play a key role in reinforcement learning, specifically in the encoding of teaching signals such as reward prediction errors (RPEs). It has been proposed that aberrant salience attribution is associated with impaired coding of RPE and heightened dopamine turnover in the striatum, and might be linked to the development of psychotic symptoms. However, the relationship of aberrant salience attribution, RPE coding, and dopamine synthesis capacity has not been directly investigated. Here we assessed the association between a behavioral measure of aberrant salience attribution, the salience attribution test, to neural correlates of RPEs measured via functional magnetic resonance imaging while healthy participants (n = 58) performed an instrumental learning task. A subset of participants (n = 27) also underwent positron emission tomography with the radiotracer [(18)F]fluoro-l-DOPA to quantify striatal presynaptic dopamine synthesis capacity. Individual variability in aberrant salience measures related negatively to ventral striatal and prefrontal RPE signals and in an exploratory analysis was found to be positively associated with ventral striatal presynaptic dopamine levels. These data provide the first evidence for a specific link between the constructs of aberrant salience attribution, reduced RPE processing, and potentially increased presynaptic dopamine function. Copyright © 2015 the authors 0270-6474/15/3510103-09$15.00/0.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 07/2015; 35(28):10103-10111. DOI:10.1523/JNEUROSCI.0805-15.2015 · 6.34 Impact Factor
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    ABSTRACT: The application of global signal regression (GSR) to resting-state functional magnetic resonance imaging data and its usefulness is a widely discussed topic. In this article, we report an observation of segregated distribution of amygdala resting-state functional connectivity (rs-FC) within the fusiform gyrus (FFG) as an effect of GSR in a multi-center-sample of 276 healthy subjects. Specifically, we observed that amygdala rs-FC was distributed within the FFG as distinct anterior versus posterior clusters delineated by positive versus negative rs-FC polarity when GSR was performed. To characterize this effect in more detail, post hoc analyses revealed the following: first, direct overlays of task-functional magnetic resonance imaging derived face sensitive areas and clusters of positive versus negative amygdala rs-FC showed that the positive amygdala rs-FC cluster corresponded best with the fusiform face area, whereas the occipital face area corresponded to the negative amygdala rs-FC cluster. Second, as expected from a hierarchical face perception model, these amygdala rs-FC defined clusters showed differential rs-FC with other regions of the visual stream. Third, dynamic connectivity analyses revealed that these amygdala rs-FC defined clusters also differed in their rs-FC variance across time to the amygdala. Furthermore, subsample analyses of three independent research sites confirmed reliability of the effect of GSR, as revealed by similar patterns of distinct amygdala rs-FC polarity within the FFG. In this article, we discuss the potential of GSR to segregate face sensitive areas within the FFG and furthermore discuss how our results may relate to the functional organization of the face-perception circuit. Hum Brain Mapp, 2015. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Human Brain Mapping 07/2015; DOI:10.1002/hbm.22900 · 5.97 Impact Factor
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    ABSTRACT: Alcohol abuse is highly prevalent, but little is understood about the molecular causes. Here, we report that Ras suppressor 1 (Rsu1) affects ethanol consumption in flies and humans. Drosophila lacking Rsu1 show reduced sensitivity to ethanol-induced sedation. We show that Rsu1 is required in the adult nervous system for normal sensitivity and that it acts downstream of the integrin cell adhesion molecule and upstream of the Ras-related C3 botulinum toxin substrate 1 (Rac1) GTPase to regulate the actin cytoskeleton. In an ethanol preference assay, global loss of Rsu1 causes high naive preference. In contrast, flies lacking Rsu1 only in the mushroom bodies of the brain show normal naive preference but then fail to acquire ethanol preference like normal flies. Rsu1 is, thus, required in distinct neurons to modulate naive and acquired ethanol preference. In humans, we find that polymorphisms in RSU1 are associated with brain activation in the ventral striatum during reward anticipation in adolescents and alcohol consumption in both adolescents and adults. Together, these data suggest a conserved role for integrin/Rsu1/Rac1/actin signaling in modulating reward-related phenotypes, including ethanol consumption, across phyla.
    Proceedings of the National Academy of Sciences 07/2015; 112(30-30):E4085-93. DOI:10.1073/pnas.1417222112 · 9.67 Impact Factor
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    ABSTRACT: Unlabelled: Theoretical and animal work has proposed that prefrontal cortex (PFC) glutamate inhibits dopaminergic inputs to the ventral striatum (VS) indirectly, whereas direct VS glutamatergic afferents have been suggested to enhance dopaminergic inputs to the VS. In the present study, we aimed to investigate relationships of glutamate and dopamine measures in prefrontostriatal circuitries of healthy humans. We hypothesized that PFC and VS glutamate, as well as their balance, are differently associated with VS dopamine. Glutamate concentrations in the left lateral PFC and left striatum were assessed using 3-Tesla proton magnetic resonance spectroscopy. Striatal presynaptic dopamine synthesis capacity was measured by fluorine-18-l-dihydroxyphenylalanine (F-18-FDOPA) positron emission tomography. First, a negative relationship was observed between glutamate concentrations in lateral PFC and VS dopamine synthesis capacity (n = 28). Second, a positive relationship was revealed between striatal glutamate and VS dopamine synthesis capacity (n = 26). Additionally, the intraindividual difference between PFC and striatal glutamate concentrations correlated negatively with VS dopamine synthesis capacity (n = 24). The present results indicate an involvement of a balance in PFC and striatal glutamate in the regulation of VS dopamine synthesis capacity. This notion points toward a potential mechanism how VS presynaptic dopamine levels are kept in a fine-tuned range. A disruption of this mechanism may account for alterations in striatal dopamine turnover as observed in mental diseases (e.g., in schizophrenia). Significance statement: The present work demonstrates complementary relationships between prefrontal and striatal glutamate and ventral striatal presynaptic dopamine using human imaging measures: a negative correlation between prefrontal glutamate and presynaptic dopamine and a positive relationship between striatal glutamate and presynaptic dopamine are revealed. The results may reflect a regulatory role of prefrontal and striatal glutamate for ventral striatal presynaptic dopamine levels. Such glutamate-dopamine relationships improve our understanding of neurochemical interactions in prefrontostriatal circuits and have implications for the neurobiology of mental disease.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 07/2015; 35(26):9615-9621. DOI:10.1523/JNEUROSCI.0329-15.2015 · 6.34 Impact Factor
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    ABSTRACT: The aim of this study was to identify if psychological distress may contribute to treatment outcome in alcohol-addicted patients during a follow-up period of 5 months after detoxification. As part of a prospective, multicenter, randomized study in relapse prevention, patients' levels of psychological distress were assessed using the Symptome Checklist (SCL-90-R). At study inclusion, all patients were detoxified and showed no more withdrawal symptoms. The patients who relapsed during the 5-month follow-up period were compared with those who remained abstinent. Predictors for relapse were investigated in a logistic regression. First, a significant difference in initial psychological distress between patients who stayed abstinent and patients who relapsed was found: following detoxification, patients who relapsed scored significantly higher on the SCL-90-R at study inclusion. In addition, psychological distress differed over time in both groups. Second, patients without relapse showed a larger decrease in some SCL-90-R scales between the beginning and the end of the observation period than patients who relapsed. Third, the logistic regression analyses showed that high scores on the overall score GSI (Global Severity Index) of the SCL-90-R can be seen as a predictor for future relapse. The SCL-90-R may be a useful instrument to predict relapse. As our study indicates that high levels of psychological distress increases the risk of relapse, specific interventions may be targeted at this risk factor. © The Author 2015. Medical Council on Alcohol and Oxford University Press. All rights reserved.
    Alcohol and Alcoholism 06/2015; DOI:10.1093/alcalc/agv062 · 2.89 Impact Factor

Publication Stats

15k Citations
2,954.70 Total Impact Points


  • 2002–2015
    • Humboldt-Universität zu Berlin
      • Department of Psychology
      Berlín, Berlin, Germany
    • Charité Universitätsmedizin Berlin
      • • Department of Psychiatry and Psychotherapy
      • • Department of Psychiatry
      Berlín, Berlin, Germany
    • University of California, Los Angeles
      • Division of Adult Psychiatry
      Los Ángeles, California, United States
  • 2000–2014
    • Central Institute of Mental Health
      • Klinik für Abhängiges Verhalten und Suchtmedizin
      Mannheim, Baden-Württemberg, Germany
    • National Institutes of Health
      베서스다, Maryland, United States
  • 2013
    • University of Greifswald
      Griefswald, Mecklenburg-Vorpommern, Germany
    • Technische Universität Dresden
      Dresden, Saxony, Germany
  • 2012
    • Bernstein Center for Computational Neuroscience Berlin
      Berlín, Berlin, Germany
  • 2011
    • University of Toronto
      • Rotman Research Institute
      Toronto, Ontario, Canada
    • University of Illinois at Chicago
      • Department of Psychology
      Chicago, Illinois, United States
  • 1990–2010
    • Ruhr-Universität Bochum
      • Neurological Clinic
      Bochum, North Rhine-Westphalia, Germany
  • 2008
    • Max Planck Institute of Psychiatry
      München, Bavaria, Germany
  • 2005–2008
    • Johannes Gutenberg-Universität Mainz
      • • Klinik und Poliklinik für Psychosomatische Medizin und Psychotherapie
      • • Institute for Nuclear Chemistry
      Mainz, Rhineland-Palatinate, Germany
  • 2007
    • Queen Mary, University of London
      • Barts and The London School of Medicine and Dentistry
      London, ENG, United Kingdom
  • 1995–2007
    • Freie Universität Berlin
      • Department of Psychiatry
      Berlín, Berlin, Germany
  • 2006
    • Universität Mannheim
      Mannheim, Baden-Württemberg, Germany
  • 2004
    • Universität Heidelberg
      Heidelburg, Baden-Württemberg, Germany
    • Bielefeld University
      Bielefeld, North Rhine-Westphalia, Germany
    • University of Hamburg
      Hamburg, Hamburg, Germany
  • 2001
    • Hannover Medical School
      Hanover, Lower Saxony, Germany
    • University of Tuebingen
      Tübingen, Baden-Württemberg, Germany
    • Royal Prince Alfred Hospital
      Camperdown, New South Wales, Australia
  • 1996–1999
    • National Institute of Mental Health (NIMH)
      • Clinical Brain Disorders Branch
      Bethesda, MD, United States