Daniel Brandeis

Universität Heidelberg, Heidelburg, Baden-Württemberg, Germany

Are you Daniel Brandeis?

Claim your profile

Publications (170)659.95 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) is associated with cognitive performance and functional brain changes that are sensitive to task conditions, indicating a role for dynamic impairments rather than stable cognitive deficits. Prominent hypotheses consistent with this observation are a failure to optimise brain arousal or activation states. Here we investigate cortical activation during different conditions. Using a sample of 41 non-comorbid adults with ADHD and 48 controls, we examine quantitative EEG activity during a resting state, a cued continuous performance test with flankers (CPT-OX) and the Sustained Attention to Response Task (SART). We further investigate the effects of methylphenidate in a subsample of 21 ADHD cases. Control participants showed a task-related increase in theta activity when engaged in cognitive tasks, primarily in frontal and parietal regions, which was absent in participants with ADHD. Treatment with methylphenidate resulted in normalisation of the resting state to task activation pattern. These findings suggest that ADHD in adults is associated with insufficient allocation of neuronal resources required for normal cortical activation commensurate with task demands. Further work is required to clarify the causal role of the deficit in cortical activation and provide a clearer understanding of the mechanisms involved.
    European Neuropsychopharmacology. 11/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Error processing and conflict monitoring are essential executive functions for goal directed actions and adaptation to conflicting information. Although medial frontal regions such as the anterior cingulate cortex (ACC) and the pre-supplementary motor area (pre-SMA) are known to be involved in these functions, there is still considerable heterogeneity regarding their spatio-temporal activations. The timing of these functions has been associated with two separable event-related potentials (ERPs) usually localized to the medial frontal wall, one during error processing (ERN - error related negativity) and one during conflict monitoring (N2). In this study we aimed to spatially and temporally dissociate conflict and error processing using simultaneously recorded EEG and fMRI data from a modified Flanker task in healthy adults. We demonstrate a spatial dissociation of conflict monitoring and error processing along the medial frontal wall, with selective conflict level dependent activation of the SMA/pre-SMA. Activation to error processing was located in the ACC, rostral cingulate zone (RCZ) and pre-SMA. The EEG-informed fMRI analysis revealed that stronger ERN amplitudes are associated with increased activation in a large coherent cluster comprising the ACC, RCZ and pre-SMA, while N2 amplitudes increased with activation in the pre-SMA. Conjunction analysis of EEG-informed fMRI revealed common activation of ERN and N2 in the pre-SMA and divergent activation in the RCZ. No conjoint activation between error processing and conflict monitoring was found with standard fMRI analysis along the medial frontal wall. Our fMRI findings clearly demonstrate that conflict monitoring and error processing are spatially dissociable along the medial frontal wall. Moreover, the overlap of ERN- and N2-informed fMRI activation in the pre-SMA provides new evidence that these ERP components share conflict related processing functions and are thus not completely separable. Copyright © 2014. Published by Elsevier Inc.
    NeuroImage 10/2014; · 6.25 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Converging evidence emphasizes the role of an interaction between monoamine oxidase A (MAOA) genotype, environmental adversity, and sex in the pathophysiology of aggression. The present study aimed to clarify the impact of this interaction on neural activity in aggression-related brain systems. Functional magnetic resonance imaging was performed in 125 healthy adults from a high-risk community sample followed since birth. DNA was genotyped for the MAOA-VNTR (variable number of tandem repeats). Exposure to childhood life stress (CLS) between the ages of 4 and 11 years was assessed using a standardized parent interview, aggression by the Youth/Young Adult Self-Report between the ages of 15 and 25 years, and the VIRA-R (Vragenlijst Instrumentele En Reactieve Agressie) at the age of 15 years. Significant interactions were obtained between MAOA genotype, CLS, and sex relating to amygdala, hippocampus, and anterior cingulate cortex (ACC) response, respectively. Activity in the amygdala and hippocampus during emotional face-matching increased with the level of CLS in male MAOA-L, while decreasing in male MAOA-H, with the reverse pattern present in females. Findings in the opposite direction in the ACC during a flanker NoGo task suggested that increased emotional activity coincided with decreased inhibitory control. Moreover, increasing amygdala activity was associated with higher Y(A)SR aggression in male MAOA-L and female MAOA-H carriers. Likewise, a significant association between amygdala activity and reactive aggression was detected in female MAOA-H carriers. The results point to a moderating role of sex in the MAOA× CLS interaction for intermediate phenotypes of emotional and inhibitory processing, suggesting a possible mechanism in conferring susceptibility to violence-related disorders.
    Cerebral cortex (New York, N.Y. : 1991). 10/2014;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Converging evidence has highlighted the association between poverty and conduct disorder (CD) without specifying neurobiological pathways. Neuroimaging research has emphasized structural and functional alterations in the orbitofrontal cortex (OFC) as one key mechanism underlying this disorder. The present study aimed to clarify the long-term influence of early poverty on OFC volume and its association with CD symptoms in healthy participants of an epidemiological cohort study followed since birth. At age 25 years, voxel-based morphometry was applied to study brain volume differences. Poverty [0=non-exposed (N=134), 1=exposed (N=33)] and smoking during pregnancy were determined using a standardized parent interview, and information on maternal responsiveness was derived from videotaped mother-infant interactions at the age of 3 months. CD symptoms were assessed by diagnostic interview from 8-19 years of age. Information on life stress was acquired at each assessment and childhood maltreatment was measured using retrospective self-report at the age of 23 years. Analyses were adjusted for sex, parental psychopathology and delinquency, obstetric adversity, parental education and current poverty. Individuals exposed to early-life poverty exhibited a lower OFC volume and more CD symptoms. Moreover, we replicated previous findings of increased CD symptoms as a consequence of childhood poverty. This effect proved statistically mediated by OFC volume and exposure to life stress and smoking during pregnancy, but not by childhood maltreatment and maternal responsiveness. These findings underline the importance of studying the impact of early-life adversity on brain alterations and highlight the need for programs to decrease income-related disparities.Neuropsychopharmacology accepted article preview online, 15 October 2014. doi:10.1038/npp.2014.277.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 10/2014; · 8.68 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: There has been an increasing interest in and the use of computer-based cognitive training as a treatment of attention-deficit/hyperactivity disorder (ADHD). The authors' review of current evidence, based partly on a stringent meta-analysis of 6 randomized controlled trials (RCTs) published in 2013, and an overview of 8 recently published RCTs highlights the inconsistency of findings between trials and across blinded and nonblinded ADHD measures within trials. Based on this, they conclude that more evidence from well-blinded studies is required before cognitive training can be supported as a frontline treatment of core ADHD symptoms.
    Child and Adolescent Psychiatric Clinics of North America 10/2014; 23(4):807-824. · 2.60 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Considerable scientific effort has been directed at developing effective treatments for attention-deficit/hyperactivity disorder (ADHD). Among alternative treatment approaches, neurofeedback has gained some promising empirical support in recent years from controlled studies as a treatment of core ADHD symptoms. However, a recent stringent meta-analysis of 8 randomized controlled trials published in 2013 found that the effects were stronger for unblinded measures and 3 recent subsequently published well-controlled trials found no effects for the most blinded ADHD outcome. Firmer conclusions must await upcoming evidence from larger controlled studies and future meta-analyses contrasting different forms of neurofeedback and different outcome measures.
    Child and adolescent psychiatric clinics of North America. 10/2014; 23(4):789-806.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Adolescence is associated with quickly changing environmental demands which require excellent adaptive skills and high cognitive flexibility. Feedback-guided adaptive learning and cognitive flexibility are driven by reward prediction error (RPE) signals, which indicate the accuracy of expectations and can be estimated using computational models. Despite the importance of cognitive flexibility during adolescence, only little is known about how RPE processing in cognitive flexibility deviates between adolescence and adulthood. In this study, we investigated the developmental aspects of cognitive flexibility by means of computational models and functional magnetic resonance imaging (fMRI). We compared the neural and behavioral correlates of cognitive flexibility in healthy adolescents (12-16years) to adults performing a probabilistic reversal learning task. Using a modified risk-sensitive reinforcement learning model, we found that adolescents learned faster from negative RPEs than adults. The fMRI analysis revealed that within the RPE network, the adolescents had a significantly altered RPE-response in the anterior insula. This effect seemed to be mainly driven by increased responses to negative prediction errors. In summary, our findings indicate that decision making in adolescence goes beyond merely increased reward-seeking behavior and provides a developmental perspective to the behavioral and neural mechanisms underlying cognitive flexibility in the context of reinforcement learning.
    NeuroImage 09/2014; · 6.25 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Elevated theta or theta/beta ratio is often reported in attention deficit hyperactivity disorder (ADHD), but the consistency across studies and the relation to hypoarousal are increasingly questioned. Reports of elevated delta related to maturational lag and of attenuated beta activity are less well replicated. Some critical inconsistencies could relate to differences in recording context. We examined if resting-state EEG power or global field synchronization (GFS) differed between recordings made at the beginning and end of a 1.5 h testing session in 76 adolescents and young adults with ADHD, and 85 controls. In addition, we aimed to examine the effect of IQ on any potential group differences. Both regional and midline electrodes yielded group main effects for delta, trends in theta, but no differences in alpha or theta/beta ratio. An additional group difference in beta was detected when using regions. Group by time interactions in delta and theta became significant when controlling for IQ. The ADHD group had higher delta and theta power at time-1, but not at time-2, whereas beta power was elevated only at time-2. GFS did not differ between groups or condition. We show some ADHD-control differences on EEG spectral power varied with recording time within a single recording session, with both IQ and electrode selection having a small but significant influence on observed differences. Our findings demonstrate the effect of recording context on resting-state EEG, and highlight the importance of accounting for these variables to ensure consistency of results in future studies.
    Brain Topography 09/2014; · 3.67 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Insensitive and unresponsive caregiving during infancy has been linked to externalizing behavior problems during childhood and adolescence. The 7-repeat (7r) allele of the dopamine D4 receptor (DRD4) gene has meta-analytically been associated with a heightened susceptibility to adverse as well as supportive environments. In the present study, we examined long-term effects of early maternal care, DRD4 genotype and the interaction thereof on externalizing and internalizing psychopathology during adolescence. As part of an ongoing epidemiological cohort study, early maternal care was assessed at child's age 3 months during a nursing and playing situation. In a sample of 296 offspring, externalizing and internalizing symptoms were assessed using a psychiatric interview conducted at age 15 years. Parents additionally filled out a questionnaire on their children's psychopathic behaviors. Results indicated that adolescents with the DRD4 7r allele who experienced less responsive and stimulating early maternal care exhibited more symptoms of ADHD and CD/ODD as well as higher levels of psychopathic behavior. In accordance with the hypothesis of differential susceptibility, 7r allele carriers showed fewer ADHD symptoms and lower levels of psychopathic behavior when exposed to especially beneficial early caregiving. In contrast, individuals without the DRD4 7r allele proved to be insensitive to the effects of early maternal care. This study replicates earlier findings with regard to an interaction between DRD4 genotype and early caregiving on externalizing behavior problems in preschoolers. It is the first one to imply continuity of this effect until adolescence.
    Journal of psychiatric research. 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) has been associated with deficient decision making and learning. Models of ADHD have suggested that these deficits could be caused by impaired reward prediction errors (RPEs). Reward prediction errors are signals that indicate violations of expectations and are known to be encoded by the dopaminergic system. However, the precise learning and decision-making deficits and their neurobiological correlates in ADHD are not well known.
    JAMA Psychiatry 08/2014; · 12.01 Impact Factor
  • Source
    Child and Adolescent Psychiatric Clinics of North America 08/2014; · 2.60 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: KEYWORDS ADHD Treatment Cognitive training Working memory Inhibitory control Attentional control Randomized controlled trial Brain plasticity KEY POINTS Cognitive training approaches, such as working memory training (WMT), are being increasingly used to target both the symptoms and the underlying neuropsychological def-icits in patients with attention-deficit/hyperactivity disorder (ADHD). The rationale of these approaches is both biologically plausible and supported by basic cognitive neuroscience. There are now 14 randomized controlled trials (RCTs) with ADHD outcomes (8 published in the past 2 years or so). At present, given the inconsistency of extant findings, more evidence from well-blinded tri-als is required before cognitive training can be supported as a frontline treatment of ADHD. Evidence in relation to improved neuropsychological function maybe more positive, but additional research is required. Future research should focus on ways to improve the content and implementation, and increase the scope, of these potentially important therapeutic approaches.
    Child and Adolescent Psychiatric Clinics of North America 08/2014; · 2.60 Impact Factor
  • Source
    Brain Topography 08/2014; 27(5):611-612. · 3.67 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Enhanced endocannabinoid signaling has been implicated in typically adolescent behavioral features such as increased risk-taking, impulsivity and novelty seeking. Research investigating the impact of genetic variants in the cannabinoid receptor 1 gene (CNR1) and of early rearing conditions has demonstrated that both factors contribute to the prediction of impulsivity-related phenotypes. The present study aimed to test the hypothesis of an interaction of the two most studied CNR1 polymorphisms rs806379 and rs1049353 with early psychosocial adversity in terms of affecting impulsivity in 15-year-olds from an epidemiological cohort sample followed since birth. In 323 adolescents (170 girls, 153 boys), problems of impulse control and novelty seeking were assessed using parent-report and self-report, respectively. Exposure to early psychosocial adversity was determined in a parent interview conducted at the age of 3 months. The results indicated that impulsivity increased following exposure to early psychosocial adversity, with this increase being dependent on CNR1 genotype. In contrast, while individuals exposed to early adversity scored higher on novelty seeking, no significant impact of genotype or the interaction thereof was detected. This is the first evidence to suggest that the interaction of CNR1 gene variants with the experience of early life adversity may play a role in determining adolescent impulsive behavior. However, given that the reported findings are obtained in a high-risk community sample, results are restricted in terms of interpretation and generalization. Future research is needed to replicate these findings and to identify the mediating mechanisms underlying this effect.
    Journal of Neural Transmission 07/2014; · 3.05 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: IMPORTANCE There is accumulating evidence relating maternal smoking during pregnancy to attention-deficit/hyperactivity disorder (ADHD) without elucidating specific mechanisms. Research investigating the neurobiological underpinnings of this disorder has implicated deficits during response inhibition. Attempts to uncover the effect of prenatal exposure to nicotine on inhibitory control may thus be of high clinical importance. OBJECTIVE To clarify the influence of maternal smoking during pregnancy (hereafter referred to as prenatal smoking) on the neural circuitry of response inhibition and its association with related behavioral phenotypes such as ADHD and novelty seeking in the mother's offspring. DESIGN, SETTING, AND PARTICIPANTS Functional magnetic resonance imaging was performed for the offspring at 25 years of age during a modified Eriksen flanker/NoGo task, and voxel-based morphometry was performed to study brain volume differences of the offspring. Prenatal smoking (1-5 cigarettes per day [14 mothers] or >5 cigarettes per day [24 mothers]) and lifetime ADHD symptoms were determined using standardized parent interviews at the offspring's age of 3 months and over a period of 13 years (from 2 to 15 years of age), respectively. Novelty seeking was assessed at 19 years of age. Analyses were adjusted for sex, parental postnatal smoking, psychosocial and obstetric adversity, maternal prenatal stress, and lifetime substance abuse. A total of 178 young adults (73 males) without current psychopathology from a community sample followed since birth (Mannheim, Germany) participated in the study. MAIN OUTCOMES AND MEASURES Functional magnetic resonance imaging response, morphometric data, lifetime ADHD symptoms, and novelty seeking. RESULTS Participants prenatally exposed to nicotine exhibited a weaker response in the anterior cingulate cortex (t168 = 4.46; peak Montreal Neurological Institute [MNI] coordinates x = -2, y = 20, z = 30; familywise error [FWE]-corrected P = .003), the right inferior frontal gyrus (t168 = 3.65; peak MNI coordinates x = 44, y = 38, z = 12; FWE-corrected P = .04), the left inferior frontal gyrus (t168 = 4.09; peak MNI coordinates x = -38, y = 36, z = 8; FWE-corrected P = .009), and the supramarginal gyrus (t168 = 5.03; peak MNI coordinates x = 64, y = -28, z = 22; FWE-corrected P = .02) during the processing of the NoGo compared to neutral stimuli, while presenting a decreased volume in the right inferior frontal gyrus. These findings were obtained irrespective of the adjustment of confounders, ADHD symptoms, and novelty seeking. There was an inverse relationship between inferior frontal gyrus activity and ADHD symptoms and between anterior cingulate cortex activity and novelty seeking. CONCLUSIONS AND RELEVANCE These findings point to a functional involvement of prenatal exposure to tobacco smoke in neural alterations similar to ADHD, which underlines the importance of smoking prevention treatments.
    JAMA Psychiatry 05/2014; · 12.01 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Accumulating evidence suggests a role of FKBP5, a co-chaperone regulating the glucocorticoid receptor sensitivity, in the etiology of depression and anxiety disorders. Based on recent findings of altered amygdala activity following childhood adversity, the present study aimed at clarifying the impact of genetic variation in FKBP5 on threat-related neural activity and coupling as well as morphometric alterations in stress-sensitive brain systems. Functional magnetic resonance imaging during an emotional face-matching task was performed in 153 healthy young adults (66 males) from a high-risk community sample followed since birth. Voxel-based morphometry was applied to study structural alterations and DNA was genotyped for FKBP5 rs1360780. Childhood adversity was measured using retrospective self-report (Childhood Trauma Questionnaire) and by a standardized parent interview assessing childhood family adversity. Depression was assessed by the Beck Depression Inventory. There was a main effect of FKBP5 on the left amygdala, with T homozygotes showing the highest activity, largest volume and increased coupling with the left hippocampus and the orbitofrontal cortex (OFC). Moreover, amygdala-OFC coupling proved to be associated with depression in this genotype. In addition, our results support previous evidence of a gene-environment interaction on right amygdala activity with respect to retrospective assessment of childhood adversity, but clarify that this does not generalize to the prospective assessment. These findings indicated that activity in T homozygotes increased with the level of adversity, whereas the opposite pattern emerged in C homozygotes, with CT individuals being intermediate. The present results point to a functional involvement of FKBP5 in intermediate phenotypes associated with emotional processing, suggesting a possible mechanism for this gene in conferring susceptibility to stress-related disorders.
    Brain Structure and Function 04/2014; · 7.84 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Frontal midline (fm-)theta activity has been related to working memory (WM) processes, as it typically increases with WM load. The robustness of this effect, however, varies across studies and subjects, putting limits to its interpretation. We hypothesized that variation in the fm-theta effect may reflect individual differences in task difficulty with increasing WM load as indicated by behavioural responses. We further tested whether effects in the alpha range are robust markers of WM load. We recorded 64-channel EEG from 24 healthy adults while they memorized either 2 or 4 unfamiliar symbols (low vs. high WM load) in a modified Sternberg task. The last 2 s of the retention phase were analyzed for WM load-related changes in the theta (5-7 Hz) and alpha range (lower: 8-10 Hz, upper: 10.5-12.5 Hz). Higher WM load led to less accurate and slower responses. The increase of fm-theta with WM load was most pronounced at fm electrodes, localized to anterior cingulate regions, and correlated with the participants' decrease in accuracy due to higher WM load. Alpha peak frequency increased in the high compared to the low WM load condition, corresponding to a decrease in lower alpha range across all channels. The results demonstrate that previously reported variation in fm-theta workload effects can partly be explained by variation in task difficulty indexed by individual task accuracy. Moreover, the results also demonstrate that alpha WM load effects are prominent when separating upper and lower alpha.
    Brain Topography 04/2014; · 3.67 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Altered very low-frequency electroencephalographic (VLF-EEG) activity is an endophenotype of ADHD in children and adolescents. We investigated VLF-EEG case-control differences in adult samples and the effects of methylphenidate (MPH). A longitudinal case-control study was conducted examining the effects of MPH on VLF-EEG (.02-0.2Hz) during a cued continuous performance task. 41 untreated adults with ADHD and 47 controls were assessed, and 21 cases followed up after MPH treatment, with a similar follow-up for 38 controls (mean follow-up=9.4months). Cases had enhanced frontal and parietal VLF-EEG and increased omission errors. In the whole sample, increased parietal VLF-EEG correlated with increased omission errors. After controlling for subthreshold comorbid symptoms, VLF-EEG case-control differences and treatment effects remained. Post-treatment, a time by group interaction emerged; VLF-EEG and omission errors reduced to the same level as controls, with decreased inattentive symptoms in cases. Reduced VLF-EEG following MPH treatment provides preliminary evidence that changes in VLF-EEG may relate to MPH treatment effects on ADHD symptoms; and that VLF-EEG may be an intermediate phenotype of ADHD. Further studies of the treatment effect of MPH in larger controlled studies are required to formally evaluate any causal link between MPH, VLF-EEG and ADHD symptoms.
    Brain and Cognition 03/2014; 86C:82-89. · 2.82 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Considerable evidence suggests that genetic factors combine with environmental influences to impact on the development of aggressive behavior. A genetic variant that has repeatedly been reported to render individuals more sensitive to the presence of adverse experiences, including stress exposure during fetal life, is the seven-repeat allele of the dopamine D4 receptor (DRD4) gene. The present investigation concentrated on the interplay of prenatal maternal stress and DRD4 genotype in predicting self-reported aggression in young adults. As disruption of the hypothalamic-pituitary-adrenal system has been discussed as a pathophysiological pathway to aggression, cortisol stress reactivity was additionally examined. As part of an epidemiological cohort study, prenatal maternal stress was assessed by maternal interview 3 months after childbirth. Between the ages of 19 and 23 years, 298 offspring (140 males, 158 females) completed the Young Adult Self-Report to measure aggressive behavior and were genotyped for the DRD4 gene. At 19 years, 219 participants additionally underwent the Trier Social Stress Test to determine cortisol reactivity. Extending earlier findings with respect to childhood antisocial behavior, the results revealed that, under conditions of higher prenatal maternal stress, carriers of the DRD4 seven-repeat allele displayed more aggression in adulthood (p = 0.032). Moreover, the same conditions which seemed to promote aggression were found to predict attenuated cortisol secretion (p = 0.028). This is the first study to indicate a long-term impact of prenatal stress exposure on the cortisol stress response depending on DRD4 genotype.
    Psychopharmacology 02/2014; · 4.06 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Difficulties with performance and brain activity related to attentional orienting (Cue-P3), cognitive or response preparation (Cue-CNV) and inhibitory response control (Nogo-P3) during tasks tapping executive functions are familial in ADHD and may represent endophenotypes. The aim of this study was to clarify the impact of dopamine receptor D4 (DRD4) and dopamine transporter (DAT1) gene polymorphisms on these processes in ADHD and control children. Behavioural and electrophysiological parameters from cued continuous performance tests with low and high attentional load were assessed in boys with ADHD combined type (N = 94) and controls without family history of ADHD (N = 31). Both groups were split for the presence of at least one DRD4 7-repeat allele and the DAT1 10-6 haplotype. Children with ADHD showed diminished performance and lower Cue-P3, CNV and Nogo-P3 amplitudes. Children with DRD4 7R showed similar performance problems and lower Cue-P3 and CNV, but Nogo-P3 was not reduced. Children with the DAT1 10-6 haplotype had no difficulties with performance or Cue-P3 and CNV, but contrary to expectations increased Nogo-P3. There were no Genotype by ADHD interactions. This study detected specific effects of DRD4 7R on performance and brain activity related to attentional orienting and response preparation, while DAT1 10-6 was associated with elevated brain activity related to inhibitory response control, which potentially compensates increased impulsivity. As these genotype effects were additive to the impact of ADHD, the current results indicate that DRD4 and DAT1 polymorphisms are functionally relevant risk factors for ADHD and presumably other disorders sharing these endophenotypes.
    Journal of Child Psychology and Psychiatry 02/2014; · 5.42 Impact Factor

Publication Stats

4k Citations
659.95 Total Impact Points


  • 2014
    • Universität Heidelberg
      • Faculty of Medicine Mannheim and Clinic Mannheim
      Heidelburg, Baden-Württemberg, Germany
  • 2003–2014
    • Central Institute of Mental Health
      • Klinik für Abhängiges Verhalten und Suchtmedizin
      Mannheim, Baden-Württemberg, Germany
  • 1985–2014
    • University of Zurich
      • • Center for Integrative Human Physiology
      • • Division of Neuropsychology
      Zürich, Zurich, Switzerland
  • 2013
    • University of Jyväskylä
      Jyväskylä, Province of Western Finland, Finland
  • 2012
    • Technische Universität Dresden
      Dresden, Saxony, Germany
  • 2007–2012
    • Universitätsmedizin Göttingen
      • Department of Child and Adolescent Psychiatry and Psychotherapy
      Göttingen, Lower Saxony, Germany
  • 2009–2011
    • King's College London
      • MRC Social, Genetic and Developmental Psychiatry Centre
      London, ENG, United Kingdom
  • 2006–2007
    • ETH Zurich
      • Institute for Biomedical Engineering
      Zürich, ZH, Switzerland
  • 1991–1992
    • San Francisco VA Medical Center
      San Francisco, California, United States