Andreas Heinz

Charité Universitätsmedizin Berlin, Berlín, Berlin, Germany

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Publications (585)2260.95 Total impact

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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; · 2.75 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.
    The Journal of nervous and mental disease. 08/2014; 202(8):623.
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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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    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
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    ABSTRACT: This article reviews the results of longitudinal studies on frontal brain volume reduction in patients with schizophrenia spectrum disorders and focuses on the relationship with antipsychotic treatment. Based on a systematic literature search all studies were included in which results on changes of brain volumes over a longer period of time were correlated with antipsychotic treatment dose and disease severity. The findings indicate that there is evidence for grey and white matter volume changes of the frontal brain, which cannot be explained by the severity of the disease alone but are also very likely a manifestation of long-term effects of antipsychotics. Whether second generation antipsychotics have an advantage compared to first generation antipsychotics is currently unclear. Considering the contribution of antipsychotics to the changes in brain structure, which seem to depend on cumulative dosage and can exert adverse effects on neurocognition, negative and positive symptoms and psychosocial functioning, the guidelines for antipsychotic long-term drug treatment should be reconsidered. This is the reason why we and others recommend prescribing the lowest dose necessary to control symptoms. In non-schizophrenic psychiatric disorders, antipsychotics should be used only with great caution after a careful risk-benefit assessment. Moreover, treatment approaches which can help to minimize antipsychotic medication or even administer them only selectively are of increasing importance.
    Der Nervenarzt 05/2014; · 0.80 Impact Factor
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    ABSTRACT: IMPORTANCE Research focusing on plasticity has shown adult neurogenesis in hippocampal subfields. Chronic alcoholism is associated with decreased plasticity and reduced whole hippocampal volume that could contribute to neuropsychiatric characteristics and outcome of the disease. OBJECTIVE To investigate the effect of alcohol abstinence on neuronal plasticity measured as longitudinal volume change in distinct hippocampal subfields. DESIGN, SETTING, AND PARTICIPANTS We acquired high-resolution structural images of 42 patients addicted to alcohol and 32 healthy control participants. Patients and control participants were both scanned twice, once after withdrawal and 2 weeks later. MAIN OUTCOMES AND MEASURES Volumes of hippocampal subfields cornu ammonis (CA) 2+3, CA4+dentate gyrus, and subiculum were determined with a user-independent segmentation method. RESULTS We found plasticity effects in bilateral CA2+3 in patients addicted to alcohol. Compared with healthy control participants, patients had lower CA2+3 volume at pretest (t31 = -0.73, P = .47) and showed a significant normalization of gray matter volume 2 weeks later. Pretest CA2+3 (t31 = -3.93, P < .001) volume was negatively associated with years of regular alcohol consumption (r42 = -0.32, P < .05) and more severe alcohol-withdrawal symptoms (r38 = -0.35, P < .05). Patients with stronger withdrawal symptoms displayed the largest volume increase of CA2+3 (r38 = 0.55, P < .001). CONCLUSIONS AND RELEVANCE The observed normalization of the bilateral hippocampal CA2+3 volume deficit matches animal data, showing a strong increase of hippocampal neurogenesis after cessation of alcohol consumption, and fits the reported increase of patients' cognitive function within a few months of alcohol abstinence. The role of CA3 in pattern separation and completion is also critical for formation of hallucinations, which constitute a severe symptom of the withdrawal syndrome. The study adds further biological arguments from structural brain research to abstain from alcohol.
    JAMA Psychiatry 05/2014; · 12.01 Impact Factor
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    ABSTRACT: Two genome-wide association studies recently showed alcohol dependence to be associated with a single-nucleotide polymorphism (rs13273672) located on a gene (GATA4) that encodes a transcription factor of atrial natriuretic peptide (ANP). A growing body of evidence suggests that ANP might be involved in the symptomology of alcohol dependence. This study examined whether reactivity to alcohol cues in the ANP target region amygdala, a key area implicated in addictive behavior, differs depending on the GATA4 genotype of a patient. We also investigated potential associations between these differences in amygdala activation and relapse behavior. Eighty-one abstinent, alcohol-dependent patients completed a functional magnetic resonance imaging cue-reactivity task in a 3-Tesla scanner and provided blood samples for DNA extraction. The results showed significantly lower alcohol-cue-induced activations in G-allele carriers as compared with AA-homozygotes in the bilateral amygdala. A survival analysis revealed that a stronger alcohol-specific amygdala response predicted a lowered risk for relapse to heavy drinking in the AA-homozygotes, whereas this effect could not be observed in G-allele carriers. These results illuminate potential underlying mechanisms of the involvement of the GATA4 gene in the etiology of alcohol dependence via its influence on ANP and amygdala processing.
    Biological Psychiatry 05/2014; 75(10):790-797. · 9.25 Impact Factor
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    ABSTRACT: Catecholamine-0-methyl-transferase (COMT) gene variation effects on prefrontal blood oxygenation-level dependent (BOLD) activation are robust; however, despite observations that COMT is oestrogenically catabolised, sex differences in its prefrontal repercussions remain unclear. Here, in a large sample of healthy adolescents stratified by sex and Val(158)Met genotype (n=1133) we examine BOLD responses during performance of the stop-signal task in right-hemispheric prefrontal regions fundamental to inhibitory control. A significant sex-by-genotype interaction was observed in pre-SMA during successful-inhibition trials and in both pre-SMA and inferior frontal cortex during failed-inhibition trials with Val-homozygotes displaying elevated activation compared to other genotypes in males but not in females. BOLD activation in the same regions significantly mediated the relationship between COMT genotype and inhibitory proficiency as indexed by stop-signal reaction time in males alone. These sexually-dimorphic effects of COMT on inhibitory brain activation have important implications for our understanding of the contrasting patterns of prefrontally-governed psychopathology observed in males and females.Neuropsychopharmacology accepted article preview online, 13 May 2014; doi:10.1038/npp.2014.107.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 05/2014; · 8.68 Impact Factor
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    ABSTRACT: Background It has been reported that mania may be associated with superior cognitive performance. In this study, we test the hypothesis that manic symptoms in youth separate along two correlated dimensions and that a symptom constellation of high energy and cheerfulness is associated with superior cognitive performance.Method We studied 1755 participants of the IMAGEN study, of average age 14.4 years (SD = 0.43), 50.7% girls. Manic symptoms were assessed using the Development and Wellbeing Assessment by interviewing parents and young people. Cognition was assessed using the Wechsler Intelligence Scale For Children (WISC-IV) and a response inhibition task.ResultsManic symptoms in youth formed two correlated dimensions: one termed exuberance, characterized by high energy and cheerfulness and one of undercontrol with distractibility, irritability and risk-taking behavior. Only the undercontrol, but not the exuberant dimension, was independently associated with measures of psychosocial impairment. In multivariate regression models, the exuberant, but not the undercontrolled, dimension was positively and significantly associated with verbal IQ by both parent- and self-report; conversely, the undercontrolled, but not the exuberant, dimension was associated with poor performance in a response inhibition task.Conclusions Our findings suggest that manic symptoms in youth may form dimensions with distinct correlates. The results are in keeping with previous findings about superior performance associated with mania. Further research is required to study etiological differences between these symptom dimensions and their implications for clinical practice.
    Journal of Child Psychology and Psychiatry 05/2014; · 5.42 Impact Factor
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    ABSTRACT: Pathological gambling (PG) shares clinical characteristics such as craving and loss of control with substance use disorders and is thus considered a behavioral addiction. While functional alterations in the mesolimbic reward system have been correlated with craving and relapse in substance use disorders, only a few studies have examined this brain circuit in PG, and no direct comparison has been conducted so far. Thus, we investigated the neuronal correlates of reward processing in PG in contrast to alcohol-dependent (AD) patients and healthy subjects. Eighteen PG patients, 15 AD patients and 17 controls were investigated with a monetary incentive delay task, in which visual cues predict the consequence (monetary gain, avoidance of loss, none) of a fast response to a subsequent target stimulus. Functional magnetic resonance imaging data were analyzed to account for possible confounding factors such as local gray matter volume. Activity in the right ventral striatum during loss anticipation was increased in PG patients compared with controls and AD patients. Moreover, PG patients showed decreased activation in the right ventral striatum and right medial prefrontal cortex during successful loss avoidance compared with controls, which was inversely associated with severity of gambling behavior. Thus, despite neurobiological similarities to substance use disorders in reward processing, as reported by previous studies, we found relevant differences with respect to the anticipation of loss as well as its avoidance (negative reinforcement), which further contributes to the understanding of PG.
    Addiction Biology 05/2014; · 5.91 Impact Factor
  • A Heinz, E Friedel
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    ABSTRACT: There are two major changes in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) concerning the field of addiction. Firstly, the previous distinction between abuse and dependence has been abolished and both disorders are now subsumed under the category addiction and related disorders. Secondly, pathological gambling has now been included in the section of addiction with slight changes in diagnostic criteria. Both changes have major implications for the definition and conceptualization of what we call a psychiatric "disease" or "disorder", which have also been addressed in the introductory statement of DSM-5. Concerning the category of abuse that is now part of substance use disorders, there is a concern that a well-defined disorder ("dependence") is now mixed with a less well-defined syndrome ("abuse"). The inclusion of non-substance, behavioral addictions poses the danger of pathologizing a wide range of human behavior in future revisions of the classification. Both concerns are further addressed in this article.
    Der Nervenarzt 04/2014; · 0.80 Impact Factor
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    ABSTRACT: Motivation is important for learning and cognition. While dopaminergic (D2) transmission in the ventral striatum (VS) is associated with motivation, learning and cognition are more strongly associated with function of the dorsal striatum, including activation in the caudate nucleus. A recent study found an interaction between intrinsic motivation and the DRD2/ANKK1 polymorphism (rs1800497), suggesting that A-carriers of rs1800497 are significantly more sensitive to motivation in order to improve during working memory (WM) training. Using data from the two large-scale imaging genetic datasets - IMAGEN (n=1080, age 13-15 years) and BrainChild (n~300, age 6-27) - we investigated whether rs1800497 is associated with WM. In the IMAGEN-dataset, we tested whether VS/caudate activation during reward anticipation was associated with WM performance and whether rs1800497 and VS/caudate activation interact to affect WM performance. We found that rs1800497 was associated with WM performance in IMAGEN and BrainChild. Higher VS and caudate activation during reward processing were significantly associated with higher WM performance (p<0.0001). An interaction was found between the DRD2/ANKK1 polymorphism rs1800497 and VS activation during reward anticipation on WM (p<0.01), such that carriers of the minor allele (A) showed a significant correlation between VS activation and WM, while the GG homozygotes did not, suggesting that the effect of VS BOLD on WM is modified by inter-individual genetic differences related to D2 dopaminergic transmission.Neuropsychopharmacology accepted article peview online, 09 April 2014; doi:10.1038/npp.2014.83.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 04/2014; · 8.68 Impact Factor
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    ABSTRACT: Variation in the CACNA1C gene has consistently been associated with psychosis in genome wide association studies. We have previously shown in a sample of n=110 healthy subjects that carriers of the CACNA1C rs1006737 risk variant exhibit hippocampal and perigenual anterior cingulate dysfunction (pgACC) during episodic memory recall. Here, we aimed to replicate our results, by testing for the effects of the rs1006737 risk variant in a new large cohort of healthy controls. We furthermore sought to refine these results by identifying the impact of a CACNA1C specific, gene-wide risk score in the absence of clinical pathology. An independent sample of 179 healthy subjects genotyped for rs1006737 underwent functional magnetic resonance imaging (fMRI) while performing an associative episodic memory task and underwent psychological testing similar to the discovery sample. The effect of gene-wide risk scores was analysed in the combined sample of 289 subjects. We replicated our discovery findings of hippocampal and pgACC dysfunction in carriers of the rs1006737 risk variant. Additionally, we observed diminished activation of the dorsolateral prefrontal cortex, in the replication sample. Our replicated results as well as this new effect were also observable in the combined sample. Moreover, the same systems-level phenotypes were significantly associated with the individual gene-based genetic risk score. Our findings suggest that altered hippocampal and frontolimbic function is associated with variants in the CACNA1C gene. Since CACNA1C variants have been associated repeatedly with psychosis at a genome-wide level, and preclinical data provide convergent evidence for the relevance of the CACNA1C gene for hippocampal and frontolimbic plasticity and adaptive regulation of stress, our data suggest a potential pathophysiological mechanism conferred by CACNA1C variants that may mediate risk for symptom dimensions shared among bipolar disorder, major depression, and schizophrenia.
    NeuroImage 03/2014; · 6.25 Impact Factor

Publication Stats

9k Citations
2,260.95 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
    • Max Planck Institute of Psychiatry
      München, Bavaria, Germany
    • Beth Israel Deaconess Medical Center
      • Department of Neurology
      Boston, MA, United States
  • 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
    • 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
    • St. Joseph's Hospital
      Savannah, Georgia, 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