Andreas Heinz

Charité Universitätsmedizin Berlin, Berlín, Berlin, Germany

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Publications (608)2347.52 Total impact

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    ABSTRACT: Previous research on alcohol dependent patients has shown that variations in eyeblink startle response can be used as an indicator of their emotional responses to alcohol-related stimuli. Postulating that reactions on substance associated stimuli are controlled by either a negative or a positive affective processing system, we expect that abstinent alcoholics react differently (within-group) in the emotional evaluation of alcohol cues. Furthermore, we assumed the startle response to covary with medication response to acamprosate and naltrexone. We measured 74 detoxified inpatients' acoustic startle responses while they were being presented with alcohol-related images as well as affectively negative, neutral, and positive pictures before they were randomized to pharmacotherapy. Group-mean startle peak amplitudes were lowest for alcohol-related cues. The relative startle response (alcohol cues set in relation to the other stimulus categories) did not correlate with craving for alcohol (OCDS) or alcohol cue induced self-ratings of arousal, valence and craving. Patients with a lower percentage of abstinent days in the 90days prior to the last drinking day showed a lower ("more appetitive") startle response to alcohol cues. A survival analysis using the time to first heavy drinking day as the survival criterion revealed a significant interaction between alcohol-cue startle responses and medication type. The results indicate that the psycho-physiological measure of emotional evaluation of alcohol cues includes unconscious processing not reflected by conscious self-ratings. Furthermore, our result of a differential medication effect may encourage further studies to use biological characteristics to stratify patients as a step towards individualized treatment for alcohol dependence.
    International journal of psychophysiology: official journal of the International Organization of Psychophysiology 12/2014; 94(3):263-71. · 3.05 Impact Factor
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    ABSTRACT: Approximately 20–30% of patients with Major depressive disorder (MDD) develop a chronic course of their disease. Chronic depression is associated with increased health care utilisation, hospitalisation and a higher disease burden. We identified clinical correlates and differences in treatment response of chronic MDD (cMDD) patients compared with non-chronic episodic depression in a huge sample of depressive inpatients.Methods Data were collected from 412 inpatients who had been diagnosed with a major depressive episode (MDE; according to ICD-10) and scored 15 or higher on the 21-item Hamilton Depression Rating Scale (HRSD-21). All subjects were participants in the German Algorithm Project, phase 3 (GAP3). Patients who were diagnosed with a MDE within the last two years or longer (herein referred to as CD) were compared with non-chronic depressive patients (herein referred to as non-CD). CD and non-CD patients were assessed for the following: psychosocial characteristics, symptom reduction from hospital admission to discharge, symptom severity at discharge, remission and response rates, and pharmacological treatment during inpatient treatment. The primary outcome measure was the HRSD-21.Results13.6% (n=56) of patients met the criteria for chronic depression. Compared with non-CD patients, patients with CD showed increased axis I comorbidities (74% vs. 52%, χ2 (1)=7.31, p=.02), a higher level of depressive symptoms at baseline and discharge, increased duration of inpatient treatment (64.8 vs. 53.3 days; t=2.86, p=.03) and lower response (HRSD: 60.0% vs. 72.0%; χ2 (1)=3.61, p<.04; BDI: 40.5% vs. 54.2%; χ2 (1)=3.56, p=.04) and remission rates (BDI 17.9.% vs. 29.7%; χ2 (1)=3.42, p=.05. However, both groups achieved a comparable symptom reduction during inpatient treatment. The prescribed pharmacological strategy had no significant influence on treatment outcome in patients with CD.Conclusion Inpatients with CD show higher symptom severity, lower response and remission rates and a longer duration of inpatient treatment, although they achieve comparable symptom reduction during treatment. These findings support the need to recognise CD and its defining characteristics as a distinct subclass of depression.
    Journal of Affective Disorders. 11/2014;
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    ABSTRACT: Background Effect sizes of pharmacotherapy in alcoholism are modest. They might improve if subjects could be divided into more homogeneous subgroups and would then be treated targeted to their neurobiological profile. In such an effort, we tested neural cue reactivity as a potential predictor of treatment response to naltrexone. Alcohol-associated cues cause brain activations in mesocorticolimbic networks due to the positive reinforcing properties of alcohol. These activations were reported to be associated with relapse behavior. Naltrexone, an antagonist at the mu-opioid receptor, improves drinking behavior in some but not all patients probably by blocking the positive reinforcement of alcohol. Conversely, acamprosate is proposed to modulate negative reinforcement (withdrawal and cue-induced withdrawal). Identifying subjects with elevated cue reactivity and testing their response to medical treatment could thus improve our understanding of some of the mechanisms underlying pharmacotherapy response.MethodsA picture-perception task featuring alcohol-related and neutral stimuli was presented to 64 recently detoxified alcohol-dependent patients. Patients came from 1 center of a larger double-blind randomized multicenter clinical trial (the “PREDICT Study”). They were scanned prior to being randomized to either naltrexone or acamprosate. We examined the interaction between medication and functional magnetic resonance imaging (fMRI) cue reactivity, as measured by the percentage of voxels activated, using the time to the first severe relapse as the outcome criterion. Our a priori formulated hypothesis was that naltrexone but not acamprosate should be efficacious in subjects with high cue reactivity.ResultsWe observed an interaction effect between pretreatment brain activation induced by alcohol images and medication (acamprosate/naltrexone) on relapse behavior. In line with our hypothesis, this interaction was driven by treatment response to naltrexone in patients with elevated pretreatment cue reactivity in the ventral striatum.ConclusionsfMRI has the potential for predicting treatment response to naltrexone in a subgroup of alcohol-dependent patients. However, this approach will be limited to researching the mechanisms and principles of treatment response.
    Alcoholism Clinical and Experimental Research 11/2014; 38(11):2754-62. · 3.42 Impact Factor
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    ABSTRACT: Prefrontal dopamine levels are relatively increased in adolescence compared to adulthood. Genetic variation of COMT (COMT Val158Met) results in lower enzymatic activity and higher dopamine availability in Met carriers. Given the dramatic changes of synaptic dopamine during adolescence, it has been suggested that effects of COMT Val158Met genotypes might have oppositional effects in adolescents and adults. The present study aims to identify such oppositional COMT Val158Met effects in adolescents and adults in prefrontal brain networks at rest. Resting state functional connectivity data were collected from cross-sectional and multicenter study sites involving 106 healthy young adults (mean age 24 ± 2.6 years), gender matched to 106 randomly chosen 14-year-olds. We selected the anterior medial prefrontal cortex (amPFC) as seed due to its important role as nexus of the executive control and default mode network. We observed a signifi-cant age-dependent reversal of COMT Val158Met effects on resting state functional connectivity between amPFC and ventrolateral as well as dorsolateral prefrontal cortex, and parahippocampal gyrus. Val homozygous adults exhibited increased and adolescents decreased connectivity compared to Met homozygotes for all reported regions. Network analyses underscored the importance of the parahippocampal gyrus as mediator of observed effects. Results of this study demonstrate that adolescent and adult resting state networks are dose-dependently and diametri-cally affected by COMT genotypes following a hypothetical model of dopamine function that follows an inverted U-shaped curve. This study might provide cues for the understanding of disease onset or dopaminergic treat-ment mechanisms in major neuropsychiatric disorders such as schizophrenia and attention deficit hyperactivity disorder.
    Brain Structure and Function 10/2014; · 7.84 Impact Factor
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    ABSTRACT: Prefrontal dopamine levels are relatively increased in adolescence compared to adulthood. Genetic variation of COMT (COMT Val158Met) results in lower enzymatic activity and higher dopamine availability in Met carriers. Given the dramatic changes of synaptic dopamine during adolescence, it has been suggested that effects of COMT Val158Met genotypes might have oppositional effects in adolescents and adults. The present study aims to identify such oppositional COMT Val158Met effects in adolescents and adults in prefrontal brain networks at rest. Resting state functional connectivity data were collected from cross-sectional and multicenter study sites involving 106 healthy young adults (mean age 24 ± 2.6 years), gender matched to 106 randomly chosen 14-year-olds. We selected the anterior medial prefrontal cortex (amPFC) as seed due to its important role as nexus of the executive control and default mode network. We observed a significant age-dependent reversal of COMT Val158Met effects on resting state functional connectivity between amPFC and ventrolateral as well as dorsolateral prefrontal cortex, and parahippocampal gyrus. Val homozygous adults exhibited increased and adolescents decreased connectivity compared to Met homozygotes for all reported regions. Network analyses underscored the importance of the parahippocampal gyrus as mediator of observed effects. Results of this study demonstrate that adolescent and adult resting state networks are dose-dependently and diametrically affected by COMT genotypes following a hypothetical model of dopamine function that follows an inverted U-shaped curve. This study might provide cues for the understanding of disease onset or dopaminergic treatment mechanisms in major neuropsychiatric disorders such as schizophrenia and attention deficit hyperactivity disorder.
    Brain Structure and Function 10/2014; · 7.84 Impact Factor
  • A Heinz
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    ABSTRACT: A disease concept should be broad enough to provide social protection for all subjects suffering from this malady but at the same time it needs to be narrow enough to avoid pathologization of behavior that is merely socially undesirable. From a medical perspective a"disease" is present if functions are impaired that are relevant for individual survival. In the field of psychiatry and psychotherapy, such medically relevant functions include the ability to be alert and fully oriented, to ascribe one's own intentions to oneself and to modulate affects according to the situation. Beyond such medically relevant symptoms of a disease, any clinically relevant dysfunction should also be harmful for the individual if a mental malady is to be diagnosed. One such harmful consequence of a disease can be that the person feels ill and suffers from this state, another negative consequence for the individual can be due to an impairment of activities of daily living and social participation. These harmful consequences of a disease are usually discussed under the heading of the"illness experience" and the"sickness aspect" of any disorder. Beyond mental maladies characterized by disease symptoms that are accompanied either by an illness experience or impaired activities of daily living and social participation (sickness), there are many states of human suffering which can be objectified and classified but do not constitute a disease in the medical sense and should more aptly be named a disorder.
    Der Nervenarzt 10/2014; · 0.80 Impact Factor
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    ABSTRACT: Human brain anatomy is strikingly diverse and highly inheritable: genetic factors may explain up to 80% of its variability. Prior studies have tried to detect genetic variants with a large effect on neuroanatomical diversity, but those currently identified account for <5% of the variance. Here, based on our analyses of neuroimaging and whole-genome genotyping data from 1765 subjects, we show that up to 54% of this heritability is captured by large numbers of single-nucleotide polymorphisms of small-effect spread throughout the genome, especially within genes and close regulatory regions. The genetic bases of neuroanatomical diversity appear to be relatively independent of those of body size (height), but shared with those of verbal intelligence scores. The study of this genomic architecture should help us better understand brain evolution and disease.Molecular Psychiatry advance online publication, 16 September 2014; doi:10.1038/mp.2014.99.
    Molecular psychiatry. 09/2014;
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    ABSTRACT: Patients with schizophrenia frequently exhibit motor deficits. However, to date, there are no studies comparing motor performance in first episode patients with schizophrenia and schizophrenia spectrum disorders (SSD; e.g. schizoaffective and brief psychosis). Participants comprised 57 first episode patients with schizophrenia, 32 first episode patients with SSD, and 51 healthy controls who underwent neuropsychological testing based on Luria׳s systematic approach, including the following tests on complex motor sequencing: the Fist-Edge-Palm (FEP) test and the bimanual probe (BP). Schizophrenia patients performed worse than SSD patients in FEP and BP, and both patient groups showed decreased scores compared to healthy controls. Furthermore, we found that a higher proportion of schizophrenia cases failed to correct their motor performance and needed external error correction, while SSD cases exhibited a higher proportion of self-correction in FEP and in BP. Lack of insight and poor executive functioning correlated with motor performance in schizophrenia, while impulse control and difficulties in abstract thinking were related to motor performance in schizophrenia spectrum disorder. Thus, psychomotor impairments appear already in first episode patients with schizophrenia and differ from impairments in SSD. Especially the inability to self-correct errors may be characteristic of schizophrenia, suggesting that impairments in error monitoring are related to psychomotor dysfunction in schizophrenia.
    Psychiatry Research 08/2014; · 2.68 Impact Factor
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    ABSTRACT: Fluid intelligence (fluid IQ), defined as the capacity for rapid problem solving and behavioral adaptation, is known to be modulated by learning and experience. Both stressful life events (SLES) and neural correlates of learning [specifically, a key mediator of adaptive learning in the brain, namely the ventral striatal representation of prediction errors (PE)] have been shown to be associated with individual differences in fluid IQ. Here, we examine the interaction between adaptive learning signals (using a well-characterized probabilistic reversal learning task in combination with fMRI) and SLES on fluid IQ measures. We find that the correlation between ventral striatal BOLD PE and fluid IQ, which we have previously reported, is quantitatively modulated by the amount of reported SLES. Thus, after experiencing adversity, basic neuronal learning signatures appear to align more closely with a general measure of flexible learning (fluid IQ), a finding complementing studies on the effects of acute stress on learning. The results suggest that an understanding of the neurobiological correlates of trait variables like fluid IQ needs to take socioemotional influences such as chronic stress into account.
    European Archives of Psychiatry and Clinical Neuroscience 08/2014; · 3.36 Impact Factor
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    ABSTRACT: Face expressions are a rich source of social signals. Here we estimated the proportion of phenotypic variance in the brain response to facial expressions explained by common genetic variance captured by ∼500,000 single nucleotide polymorphisms. Using genomic-relationship-matrix restricted maximum likelihood (GREML), we related this global genetic variance to that in the brain response to facial expressions, as assessed with functional magnetic resonance imaging (fMRI) in a community-based sample of adolescents (n = 1,620). Brain response to facial expressions was measured in 25 regions constituting a face network, as defined previously. In 9 out of these 25 regions, common genetic variance explained a significant proportion of phenotypic variance (40-50%) in their response to ambiguous facial expressions; this was not the case for angry facial expressions. Across the network, the strength of the genotype-phenotype relationship varied as a function of the inter-individual variability in the number of functional connections possessed by a given region (R2 = 0.38, p<0.001). Furthermore, this variability showed an inverted U relationship with both the number of observed connections (R2 = 0.48, p<0.001) and the magnitude of brain response (R2 = 0.32, p<0.001). Thus, a significant proportion of the brain response to facial expressions is predicted by common genetic variance in a subset of regions constituting the face network. These regions show the highest inter-individual variability in the number of connections with other network nodes, suggesting that the genetic model captures variations across the adolescent brains in co-opting these regions into the face network.
    PLoS Genetics 08/2014; 10(8):e1004523. · 8.52 Impact Factor
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    ABSTRACT: The authors report the development of psychosis in a young woman coinciding with excessive use of the online communication system Twitter and the results of an experimental account to argue that Twitter may have a high potential to induce psychosis in predisposed users.
    Journal of Nervous & Mental Disease 08/2014; 202(8):623. · 1.84 Impact Factor
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    ABSTRACT: Objective The authors sought to model the unique and common variance across conduct disorder, substance misuse, and attention deficit hyperactivity disorder (ADHD) and to investigate the neurocognitive factors that relate generally or uniquely to externalizing problems in adolescence. Method Personality and behavioral measures and functional imaging responses to reward sensitivity and response inhibition tasks were assessed in 1,778 European adolescents at age 14 and, using structural equation modeling, were related to the unique and common variance across externalizing problems assessed and modeled at ages 14 and 16. Results Externalizing problems best fit a general-specific model made up of a specific factor representing ADHD and conduct disorder symptoms, a specific factor representing substance misuse symptoms, and a common externalizing factor representing the variance shared among all symptoms. Common variance across externalizing problems was associated with high impulsivity and delay discounting as well as low blood-oxygen-level-dependent (BOLD) response in the substantia nigra and subthalamic nucleus but high BOLD response in the presupplementary motor area and precentral gyrus during successful inhibition. Unique variance for ADHD/conduct disorder was associated with impulsivity, poor response inhibition, and high delay discounting, as well as low BOLD response in frontal brain areas bilaterally during failed inhibition. In contrast, unique variance for substance misuse was associated with high sensation seeking and delay discounting, as well as differential brain response to reward anticipation: high BOLD response in the left orbitofrontal cortex but low BOLD response in the left inferior frontal gyrus. Conclusions Personality, behavioral, and fMRI findings suggest that abnormalities in response inhibition, error processing, and reward processing are differentially implicated in underlying vulnerability specific to ADHD/conduct disorder and substance misuse and general to externalizing problems.
    American Journal of Psychiatry 07/2014; · 14.72 Impact Factor
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    ABSTRACT: The fronto-limbic network interaction, driven by glutamatergic and dopaminergic neurotransmission, represents a core mechanism of motivated behavior and personality traits. Reward seeking behavior undergoes tremendous changes in adolescence paralleled by neurobiological changes of this network including the prefrontal cortex, striatum and amygdala. Since fronto-limbic dysfunctions also underlie major psychiatric diseases beginning in adolescence, this investigation focuses on network characteristics separating adolescents from adults. To investigate differences in network interactions, the brain reward system activity (slot machine task) together with frontal glutamate concentration (anterior cingulate cortex, ACC) was measured in 28 adolescents and 26 adults employing functional magnetic resonance imaging and magnetic resonance spectroscopy, respectively. An inverse coupling of glutamate concentrations in the ACC and activation of the ventral striatum was observed in adolescents. Further, amygdala response in adolescents was negatively correlated with the personality trait impulsivity. For adults, no significant associations of network components or correlations with impulsivity were found. The inverse association between frontal glutamate concentration and striatal activation in adolescents is in line with the triadic model of motivated behavior stressing the important role of frontal top-down inhibition on limbic structures. Our data identified glutamate as the mediating neurotransmitter of this inhibitory process and demonstrates the relevance of glutamate on the reward system and related behavioral traits like impulsivity. This fronto-limbic coupling may represent a vulnerability factor for psychiatric disorders starting in adolescence but not in adulthood.
    Brain Structure and Function 07/2014; · 7.84 Impact Factor
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    ABSTRACT: A comprehensive account of the causes of alcohol misuse must accommodate individual differences in biology, psychology and environment, and must disentangle cause and effect. Animal models1 can demonstrate the effects of neurotoxic substances; however, they provide limited insight into the psycho-social and higher cognitive factors involved in the initiation of substance use and progression to misuse. One can search for pre-existing risk factors by testing for endophenotypic biomarkers2 in non-using relatives; however, these relatives may have personality or neural resilience factors that protect them from developing dependence3. A longitudinal study has potential to identify predictors of adolescent substance misuse, particularly if it can incorporate a wide range of potential causal factors, both proximal and distal, and their influence on numerous social, psychological and biological mechanisms4. Here we apply machine learning to a wide range of data from a large sample of adolescents (n = 692) to generate models of current and future adolescent alcohol misuse that incorporate brain structure and function, individual personality and cognitive differences, environmental factors (including gestational cigarette and alcohol exposure), life experiences, and candidate genes. These models were accurate and generalized to novel data, and point to life experiences, neurobiological differences and personality as important antecedents of binge drinking. By identifying the vulnerability factors underlying individual differences in alcohol misuse, these models shed light on the aetiology of alcohol misuse and suggest targets for prevention.
    Nature 07/2014; · 38.60 Impact Factor
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    ABSTRACT: A dimensional approach in psychiatry aims to identify core mechanisms of mental disorders across nosological boundaries.
    Psychopharmacology 06/2014; · 4.06 Impact Factor
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    ABSTRACT: Functional interactions between the dorsolateral prefrontal cortex and hippocampus during working memory have been studied extensively as an intermediate phenotype for schizophrenia. Coupling abnormalities have been found in patients, their unaffected siblings, and carriers of common genetic variants associated with schizophrenia, but the global genetic architecture of this imaging phenotype is unclear. To achieve genome-wide hypothesis-free identification of genes and pathways associated with prefrontal-hippocampal interactions, we combined gene set enrichment analysis with whole-genome genotyping and functional magnetic resonance imaging data from 269 healthy German volunteers. We found significant enrichment of the synapse organization and biogenesis gene set. This gene set included known schizophrenia risk genes, such as neural cell adhesion molecule (NRCAM) and calcium channel, voltage-dependent, beta 2 subunit (CACNB2), as well as genes with well-defined roles in neurodevelopmental and plasticity processes that are dysfunctional in schizophrenia and have mechanistic links to prefrontal-hippocampal functional interactions. Our results demonstrate a readily generalizable approach that can be used to identify the neurogenetic basis of systems-level phenotypes. Moreover, our findings identify gene sets in which genetic variation may contribute to disease risk through altered prefrontal-hippocampal functional interactions and suggest a link to both ongoing and developmental synaptic plasticity.
    Proceedings of the National Academy of Sciences of the United States of America. 06/2014;
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    ABSTRACT: Background / Purpose: The aim of this work was to investigate the neural association of goal-directed and habitual behavioral control, in a two-stage Markov decision task, with two behavioral measures of discounting. We correlated neural activation co-varying with model-free and model-based reward prediction errors, with parameters for delay and probability discounting in a sample of 55 healthy men at age 18. Main conclusion: Model-based reward prediction error signals in striatum are associated with probability discounting in a way that suggests more risk-seeking persons to have weaker model-based reinforcement learning.
    Annual Meeting of the Organization for Human Brain Mapping, Hamburg; 06/2014
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    ABSTRACT: Individuals with alcohol-dependent parents show an elevated risk of developing alcohol-related problems themselves. Modulations of the mesolimbic reward circuit have been postulated as a pre-existing marker of alcoholism. We tested whether a positive family history of alcoholism is correlated with ventral striatum functionality during a reward task. All participants performed a modified version of the monetary incentive delay task while their brain responses were measured with functional magnetic resonance imaging. We compared 206 healthy adolescents (aged 13-15) who had any first- or second-degree relative with alcoholism to 206 matched controls with no biological relative with alcoholism. Reward anticipation as well as feedback of win recruited the ventral striatum in all participants, but adolescents with a positive family history of alcoholism did not differ from their matched peers. Also we did not find any correlation between family history density and reward anticipation or feedback of win. This finding of no differences did not change when we analyzed a subsample of 77 adolescents with at least one parent with alcohol use disorder and their matched controls. Because this result is in line with another study reporting no differences between children with alcohol-dependent parents and controls at young age, but contrasts with studies of older individuals, one might conclude that at younger age the effect of family history has not yet exerted its influence on the still developing mesolimbic reward circuit.
    Addiction Biology 06/2014; · 5.91 Impact Factor
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    ABSTRACT: The s/s-genotype of the 5-HTTLPR polymorphism and the personality trait of neuroticism have both been associated with experiences of negative affect, anxiety and mood disorders, as well as an emotional processing bias towards negative facial emotions. On a neural level, this bias can be characterized by altered amygdala and fusiform gyrus (FFG) activity during perception of negative facial expressions. Using resting-state functional magnetic resonance imaging in a multi-center-sample of 178 healthy subjects of European descent, this study investigated the association of 5-HTTLPR (short s- and long l-allele) including the genotype of the single nucleotide polymorphism (SNP) rs25531 (A/G) within this region polymorphism, and trait neuroticism on resting-state functional connectivity (rs-FC) between amygdala and the FFG. Moreover, we aimed to identify additional brain regions with associations of 5-HTTLPR/rs25531 (combined according to its expression; low: s/s; high: lA/lA; intermediate: s/lA, s/lG, lG/lG, lA/lG) and trait neuroticism to amygdala rs-FC. Separate analyses for 5-HTTLPR/rs25531 and neuroticism (controlling for age, gender, handedness, and research site) revealed that s/s-homozygotes and individuals high in neuroticism obtained altered amygdala rs-FC in the right occipital face area, which is considered to be a "core component" of the face processing system. Importantly, effects of neuroticism were replicated across three independent research sites. Additionally, associations of 5-HTTLPR/rs25531 genotype and amygdala rs-FC were observed in the anterior and posterior cingulate cortex, whereas neuroticism was not related to rs-FC in these areas. The presented data implies that 5-HTTLPR/rs25531 variants and neuroticism are linked by resting state functional connectivity of amygdala and fusiform gyrus and suggests that variants of 5-HTTLPR/rs25531 genotype and different levels of neuroticism may partly account for altered processing of negative facial emotions.
    Brain Structure and Function 05/2014; · 7.84 Impact Factor

Publication Stats

10k Citations
2,347.52 Total Impact Points

Institutions

  • 2002–2014
    • Charité Universitätsmedizin Berlin
      • • Department of Psychiatry and Psychotherapy
      • • Department of Anesthesiology and Operative Intensive Care Medicine
      • • Department of Psychiatry
      Berlín, Berlin, Germany
  • 2013
    • University of Greifswald
      Griefswald, Mecklenburg-Vorpommern, Germany
    • Universität Potsdam
      Potsdam, Brandenburg, Germany
  • 2008–2013
    • Aarhus University
      • Centre of Functionally Integrative Neuroscience CFIN
      Århus, Central Jutland, Denmark
    • King's College London
      • • MRC Social, Genetic and Developmental Psychiatry Centre
      • • Institute of Psychiatry
      Londinium, England, United Kingdom
    • Beth Israel Deaconess Medical Center
      • Department of Neurology
      Boston, MA, United States
    • Max Planck Institute of Psychiatry
      München, Bavaria, Germany
  • 2007–2013
    • Technische Universität Dresden
      Dresden, Saxony, Germany
    • Universitatea de Medicina si Farmacie Craiova
      Croiova, Dolj, Romania
  • 2012
    • Kliniken Essen-Mitte Knappschafts-Krankenhaus
      Essen, North Rhine-Westphalia, Germany
  • 2000–2012
    • Humboldt-Universität zu Berlin
      • Department of Psychology
      Berlín, Berlin, Germany
    • Central Institute of Mental Health
      • Klinik für Abhängiges Verhalten und Suchtmedizin
      Mannheim, Baden-Württemberg, Germany
    • National Institutes of Health
      Maryland, United States
  • 2011
    • North Shore-Long Island Jewish Health System
      New York City, New York, United States
    • Ghent University
      • Department of Experimental Psychology
      Merelbeke, VLG, Belgium
    • University Medical Center Hamburg - Eppendorf
      • Department of Systems Neuroscience
      Hamburg, Hamburg, Germany
    • University of Illinois at Chicago
      • Department of Psychology
      Chicago, IL, United States
  • 2005–2011
    • University of Tuebingen
      Tübingen, Baden-Württemberg, Germany
    • Universitätsklinikum Freiburg
      • Center for Mental Illness
      Freiburg, Lower Saxony, Germany
  • 2001–2011
    • Universität Heidelberg
      • Central Institute of Mental Health
      Heidelberg, Baden-Wuerttemberg, Germany
    • Royal Prince Alfred Hospital
      Camperdown, New South Wales, Australia
    • Heidelberg University
      Tiffin, Ohio, United States
  • 1990–2011
    • Ruhr-Universität Bochum
      • Neurologische Klinik
      Bochum, North Rhine-Westphalia, Germany
  • 2009
    • Centre for Addiction and Mental Health
      Toronto, Ontario, Canada
    • Technische Universität Berlin
      • School IV Electrical Engineering and Computer Science
      Berlin, Land Berlin, Germany
  • 2007–2008
    • Queen Mary, University of London
      • Barts and The London School of Medicine and Dentistry
      Londinium, England, United Kingdom
  • 2006–2008
    • Johannes Gutenberg-Universität Mainz
      • • Klinik und Poliklinik für Psychosomatische Medizin und Psychotherapie
      • • Institute for Nuclear Chemistry
      Mainz, Rhineland-Palatinate, Germany
    • Saint Joseph Hospital
      Chicago, Illinois, United States
  • 1994–2006
    • Freie Universität Berlin
      • Department of Psychiatry
      Berlín, Berlin, Germany
  • 2000–2005
    • National Institute on Alcohol Abuse and Alcoholism
      Maryland, United States
  • 1996–1999
    • National Institute of Mental Health (NIMH)
      • Clinical Brain Disorders Branch
      Bethesda, MD, United States
  • 1992
    • St. Josef-Hospital
      Bonn, North Rhine-Westphalia, Germany