René S Kahn

University Medical Center Utrecht, Utrecht, Utrecht, Netherlands

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Publications (501)2670.54 Total impact

  • Journal of clinical psychopharmacology 04/2013; 33(2):258-261. · 5.09 Impact Factor
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    ABSTRACT: BACKGROUND: Cognitive deficits have been recognized as a key feature of schizophrenia, since the first description by Kraepelin. Specifically, lower intelligence is considered a core feature of the disorder and may represent a risk factor for its development. However, whether global intelligence decreases over time in schizophrenia is not known. The aims of this quantitative meta-analysis are to gather, integrate and estimate the overall mean effect size of IQ change over time in schizophrenia as compared to healthy individuals. METHODS: A systematic search was conducted to identify relevant studies. Longitudinal studies with at least two intelligence assessments in schizophrenia cohorts were retrieved. Studies had to report sufficient data on IQ-change and include data from healthy comparisons for computation of effect sizes. For each study, the Cohen d was calculated as well as a combined mean effect size. RESULTS: Fourteen studies were identified. Eight studies with a total of 280 patients and 306 healthy controls were suitable to be included. The mean weighted baseline IQ was 97.20 for patients and 109.26 for controls. The mean weighted IQ-change per year was +0.33 for patients and +2.08 for controls. The combined effect size was Cohen's d=-0.48, p=0.01. CONCLUSIONS: A global cognitive deficit is present in patients with schizophrenia expressed as a lower test score increase over repeated testing as compared to healthy subjects possibly due to the lack of practice effects in patients. Thus, schizophrenia is characterized by a relative lack of gain in global cognitive abilities over time.
    Schizophrenia Research 03/2013; · 4.59 Impact Factor
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    ABSTRACT: INTRODUCTION: Verbal auditory hallucinations (VAHs) are experienced as spoken voices which seem to originate in the extracorporeal environment or inside the head. Animal and human research has identified a 'where' pathway for sound processing comprising the planum temporale, the middle frontal gyrus and the inferior parietal lobule. We hypothesize that increased activity of that 'where' pathway mediates the exteriorization of VAHs. METHODS: The fMRI scans of 52 right-handed psychotic patients experiencing frequent VAHs were compared with the reported location of hallucinations, as rated with the aid of the PSYRATS-AHRS. For each subject, a unique VAH activation model was created based on the VAH timings, and subsequently convolved with a gamma function to model the hemodynamic response. In order to examine the neurofunctional equivalents of perceived VAH location, second-level group effects of subjects experiencing either internal (n=24) or external (n=28) VAHs were contrasted within planum temporale, middle frontal gyrus, and inferior parietal lobule regions of interest (ROIs). RESULTS: Three ROIs were tested for increased activity in relation with the exteriorization of VAHs. The analysis revealed a left-sided medial planum temporale and a right-sided middle frontal gyrus cluster of increased activity. No significant activity was found in the inferior parietal lobule. CONCLUSIONS: Our study indicates that internal and external VAHs are mediated by a fronto-temporal pattern of neuronal activity while the exteriorization of VAHs stems from additional brain activity in the auditory 'where' pathway, comprising the planum temporale and prefrontal regions.
    Schizophrenia Research 03/2013; · 4.59 Impact Factor
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    ABSTRACT: Decisions are rarely made in social isolation. One phenomenon often observed in social interactions is altruistic punishment, i.e. the punishment of unfair behavior by others at a personal cost. The tendency for altruistic punishment is altered by affective states including those induced by stress exposure. Stress is thought to exert bi-directional effects on behavior: immediately after stress, reflex-like and habitual behavior is promoted while later on more far-sighted, flexible and goal-directed behavior is enhanced. We hypothesized that such time-dependent effects of stress would also be present in the context of altruistic punishment behavior. Healthy male participants (N=80) were exposed to either a grouped stress test or a control condition. Participants were tested in prosocial decision making tasks either directly after stress or 75min later. Altruistic punishment was assessed using the Ultimatum Game. General altruism was assessed with a one-shot version of the Dictator Game in which an anonymous donation could be offered to a charitable organization. We found that stress caused a bi-directional effect on altruistic punishment, with decreased rejection rates in the late aftermath of stress in response to ambiguous 30% offers. In the Dictator Game, stressed participants were less generous than controls, but no time-dependent effect was observed, indicating that the general reward sensitivity remained unchanged at various time-points after stress. Overall, during the late aftermath after acute stress exposure (i.e. 75min later), participants acted more consistent with their own material self-interest, and had a lower propensity for altruistic punishment, possibly through upregulation of cognitive self-control mechanisms. Thus, our findings underscore the importance of time as a factor in simple, real-life economic decisions in a stressful social context.
    Psychoneuroendocrinology 01/2013; · 5.59 Impact Factor
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    ABSTRACT: In psychiatric disorders, the effect of genetic and environmental factors may converge on molecular pathways and brain circuits related to growth factor functioning. In this review, we describe how disturbances in fibroblast growth factors (FGFs) and their receptors influence behavior by affecting brain development. Recently, several studies reported associations of members of the FGF family with psychiatric disorders. FGFs are key candidates to modulate the impact of environmental factors, such as stress. Mutant mice for FGF receptor 1 show schizophrenia-like behaviors that are related to general loss of neurons and postnatal glia dysfunction. Mice lacking FGF2, a FGFR1 ligand, show similar reductions in brain volume and hyperactivity, as well as increased anxiety behaviors. FGFR2 and FGF17 are involved in the development of frontal brain regions and impairments in cognitive and social behaviors, respectively. Moreover, treatment with FGF2 was beneficial for depressive and cognitive measures in several animal studies and one human study. These findings indicate the importance of the FGF system with respect to developing novel etiology-directed treatments for psychopathology.
    The Neuroscientist 01/2013; · 5.63 Impact Factor
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    ABSTRACT: Genomic copy number variations (CNVs) and increased parental age are both associated with the risk to develop a variety of clinical neuropsychiatric disorders such as autism, schizophrenia and bipolar disorder. At the same time, it has been shown that the rate of transmitted de novo single nucleotide mutations is increased with paternal age. To address whether paternal age also affects the burden of structural genomic deletions and duplications, we examined various types of CNV burden in a large population sample from the Netherlands. Healthy participants with parental age information (n = 6,773) were collected at different University Medical Centers. CNVs were called with the PennCNV algorithm using Illumina genome-wide SNP array data. We observed no evidence in support of a paternal age effect on CNV load in the offspring. Our results were negative for global measures as well as several proxies for de novo CNV events in this unique sample. While recent studies suggest de novo single nucleotide mutation rate to be dominated by the age of the father at conception, our results strongly suggest that at the level of global CNV burden there is no influence of increased paternal age. While it remains possible that local genomic effects may exist for specific phenotypes, this study indicates that global CNV burden and increased father's age may be independent disease risk factors.
    Human Genetics 01/2013; · 4.63 Impact Factor
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    ABSTRACT: For most complex traits, results from genome-wide association studies show that the proportion of the phenotypic variance attributable to the additive effects of individual SNPs, that is, the heritability explained by the SNPs, is substantially less than the estimate of heritability obtained by standard methods using correlations between relatives. This difference has been called the "missing heritability". One explanation is that heritability estimates from family (including twin) studies are biased upwards. Zuk et al. revisited overestimation of narrow sense heritability from twin studies as a result of confounding with non-additive genetic variance. They propose a limiting pathway (LP) model that generates significant epistatic variation and its simple parametrization provides a convenient way to explore implications of epistasis. They conclude that over-estimation of narrow sense heritability from family data ('phantom heritability') may explain an important proportion of missing heritability. We show that for highly heritable quantitative traits large phantom heritability estimates from twin studies are possible only if a large contribution of common environment is assumed. The LP model is underpinned by strong assumptions that are unlikely to hold, including that all contributing pathways have the same mean and variance and are uncorrelated. Here, we relax the assumptions that underlie the LP model to be more biologically plausible. Together with theoretical, empirical, and pragmatic arguments we conclude that in outbred populations the contribution of additive genetic variance is likely to be much more important than the contribution of non-additive variance.
    PLoS ONE 01/2013; 8(7):e68913. · 3.53 Impact Factor
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    ABSTRACT: Cognitive tasks that do not change the required response for a stimulus over time ('consistent mapping') show dramatically improved performance after relative short periods of practice. This improvement is associated with reduced brain activity in a large network of brain regions, including left prefrontal and parietal cortex. The present study used fMRI-guided repetitive transcranial magnetic stimulation (rTMS), which has been shown to reduce processing efficacy, to examine if the reduced activity in these regions also reflects reduced involvement, or possibly increased efficiency. First, subjects performed runs of a Sternberg task in the scanner with novel or practiced target-sets. This data was used to identify individual sites for left prefrontal and parietal peak brain activity, as well as to examine the change in activity related to practice. Outside of the scanner, real and sham rTMS was applied at left prefrontal and parietal cortex to examine their involvement novel and practiced conditions. Prefrontal as well as parietal rTMS significantly reduced target accuracy for novel targets. Prefrontal, but not parietal, rTMS interference was significantly lower for practiced than novel target-sets. rTMS did not affect non-target accuracy, or reaction time in any condition. These results show that task practice in a consistent environment reduces involvement of the prefrontal cortex. Our findings suggest that prefrontal cortex is predominantly involved in target maintenance and comparison, as rTMS interference was only detectable for targets. Findings support process switching hypotheses that propose that practice creates the possibility to select a response without the need to compare with target items. Our results also support the notion that practice allows for redistribution of limited maintenance resources.
    PLoS ONE 01/2013; 8(12):e80256. · 3.53 Impact Factor
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    ABSTRACT: Evidence is increasing for involvement of the endocannabinoid system in cognitive functions including attention and executive function, as well as in psychiatric disorders characterized by cognitive deficits, such as schizophrenia. Executive function appears to be associated with both modulation of active networks and inhibition of activity in the default mode network. In the present study, we examined the role of the endocannabinoid system in executive function, focusing on both the associated brain network and the default mode network. A pharmacological functional magnetic resonance imaging (fMRI) study was conducted with a placebo-controlled, cross-over design, investigating effects of the endocannabinoid agonist Δ9-tetrahydrocannabinol (THC) on executive function in 20 healthy volunteers, using a continuous performance task with identical pairs. Task performance was impaired after THC administration, reflected in both an increase in false alarms and a reduction in detected targets. This was associated with reduced deactivation in a set of brain regions linked to the default mode network, including posterior cingulate cortex and angular gyrus. Less deactivation was significantly correlated with lower performance after THC. Regions that were activated by the continuous performance task, notably bilateral prefrontal and parietal cortex, did not show effects of THC. These findings suggest an important role for the endocannabinoid system in both default mode modulation and executive function. This may be relevant for psychiatric disorders associated with executive function deficits, such as schizophrenia and ADHD.
    PLoS ONE 01/2013; 8(7):e70074. · 3.53 Impact Factor
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    ABSTRACT: In order to assess the importance of environmental and genetic risk on transition from health to psychotic disorder, a prospective study of individuals at average (n = 462) and high genetic risk (n = 810) was conducted. A three-year cohort study examined the rate of transition to psychotic disorder. Binary measures indexing environmental exposure (combining urban birth, cannabis use, ethnicity and childhood trauma) and proxy genetic risk (high-risk sibling status) were used to model transition. The majority of high-risk siblings (68%) and healthy comparison subjects (60%) had been exposed to one or more environmental risks. The risk of transition in siblings (n = 9, 1.1%) was higher than the risk in healthy comparison subjects (n = 2, 0.4%; ORadj = 2.2,95%CI:5-10.3). All transitions (100%) were associated with environmental exposure, compared to 65% of non-transitions (p = 0.014), with the greatest effects for childhood trauma (ORadj = 34.4,95%CI:4.4-267.4), cannabis use (OR = 4.1,95%CI:1.1, 15.4), minority ethnic group (OR = 3.8,95%CI:1.2,12.8) and urban birth (OR = 3.7,95%CI:0.9,15.4). The proportion of transitions in the population attributable to environmental and genetic risk ranged from 28% for minority ethnic group, 45% for urban birth, 57% for cannabis use, 86% for childhood trauma, and 50% for high-risk sibling status. Nine out of 11 transitions (82%) were exposed to both genetic and environmental risk, compared to only 43% of non-transitions (p = 0.03). Environmental risk associated with transition to psychotic disorder is semi-ubiquitous regardless of genetic high risk status. Careful prospective documentation suggests most transitions can be attributed to powerful environmental effects that become detectable when analysed against elevated background genetic risk, indicating gene-environment interaction.
    PLoS ONE 01/2013; 8(11):e76690. · 3.53 Impact Factor
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    ABSTRACT: In a previous study we reported on a non-invasive functional diffusion tensor imaging (fDTI) method to measure neuronal signals directly from subtle changes in fractional anisotropy along white matter tracts. We hypothesized that these fractional anisotropy changes relate to morphological changes of glial cells induced by axonal activity. In the present study we set out to replicate the results of the previous study with an improved fDTI scan acquisition scheme. A group of twelve healthy human participants were scanned on a 3 Tesla MRI scanner. Activation was revealed in the contralateral thalamo-cortical tract and optic radiations during tactile and visual stimulation, respectively. Mean percent signal change in FA was 3.47% for the tactile task and 3.79% for the visual task, while for the MD the mean percent signal change was only -0.10 and -0.09%. The results support the notion of different response functions for tactile and visual stimuli. With this study we successfully replicated our previous findings using the same types of stimuli but on a different group of healthy participants and at different field-strength. The successful replication of our first fDTI results suggests that the non-invasive fDTI method is robust enough to study the functional neural networks in the human brain within a practically feasible time period.
    Frontiers in Human Neuroscience 01/2013; 7:817. · 2.91 Impact Factor
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    ABSTRACT: A putative pathway by which the BDNF Val66Met polymorphism (rs6265) leads to aberrant phenotypes is its influence on plasma BDNF. Research into the impact of rs6265 on plasma BDNF has given rise to conflicting results. Moreover, most such studies have compared Met-carriers with Val-homozygous subjects. We therefore genotyped subjects from a population-based cohort (the Utrecht Health Project, N=2,743) and assessed whether plasma BDNF differs between rs6265 homozygous groups. We maximized the number of Met-homozygous subjects in whom we measured plasma BDNF, resulting in plasma BDNF being available for 19 Met-homozygous and 42 matched Val-homozygous subjects. Mean concentrations (S.D.) were 1963.1 (750.1) and 2133.2 pg/ml (1164.3) for the Val/Val and Met/Met groups, respectively. Using ANOVA, no differences in plasma BDNF between the two groups were detected. In conclusion, these results add to a growing body of evidence indicating that allelic variation at rs6265 does not have medium to large effects on plasma BDNF concentrations.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 12/2012; 43:185. · 3.55 Impact Factor
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    ABSTRACT: Available data on antipsychotic-induced metabolic risks are often constrained by potential confounding effects due to prior antipsychotic treatment. In this study, we assessed the baseline prevalence of metabolic abnormalities and changes following treatment with five commonly-used antipsychotic drugs (haloperidol, amisulpride, olanzapine, quetiapine or ziprasidone) in first-episode, partially antipsychotic-naive patients with schizophrenia in the European first-episode schizophrenia trial (EUFEST). Overall baseline prevalence of metabolic syndrome (MetS) was 6.0%, with similar rates observed in the antipsychotic-naive patients (5.7%, 9/157) and in the other patients with only a brief prior exposure to antipsychotics (6.1%, 20/326). These results are consistent with the MetS prevalence rate estimated in a general population of similar age. Examination of individual risk factors showed 58.5% of subjects had one or more elevated metabolic risks at baseline: 28.5% demonstrated suboptimal HDL; 24.2% hypertension; 17.7% hypertriglyceridemia; 8.2% abdominal obesity; 7.3% hyperglycaemia. Increase in body weight (kg/month) occurred in patients treated with haloperidol (0.62 s.e. 0.11), amisulpride (0.76 s.e. 0.08), olanzapine (0.98 s.e. 0.07) and quetiapine (0.58 s.e. 0.09), which was significantly greater than that in the ziprasidone group (0.18 s.e. 0.10). The incidence rate of new diabetes cases over a 52-wk follow-up period was 0.82% (4/488). More patients experienced worsening rather than improvement of hypertriglyceridemia or hyperglycaemia in all treatment groups. Our findings suggest that in first-episode, partially antipsychotic-naive patients, the baseline prevalence rate of MetS appears to be no higher than that in the general population, but serious underlying individual risk factors nevertheless existed.
    The International Journal of Neuropsychopharmacology 12/2012; · 5.64 Impact Factor
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    ABSTRACT: The similarity between aspects of the clinical presentation of schizophrenia and autism spectrum disorders (ASD) suggests that elements of the biological etiology may also be shared between these two disorders. Recently, an increasing number of rare, mostly structural genetic variants are reported to increase the risk of both schizophrenia and ASD. We hypothesized that given this evidence for a shared genetic background based on rare genetic variants, common risk alleles may also be shared between ASD and schizophrenia. To test this hypothesis, the polygenic score, which summarizes the collective effect of a large number of common risk alleles, was used. We examined whether the polygenic score derived from a schizophrenia case-control dataset, previously reported by Purcell et al., was able to differentiate ASD cases from controls. The results demonstrate that the schizophrenia-derived polygenic score is not different between ASD cases and controls, indicating that there is no important sharing of common risk alleles between the two neuropsychiatric disorders. Possibly, common risk alleles are less important in ASD in comparison to their more prominent role in schizophrenia and bipolar disorders. These findings provide important novel insights into shared and distinct elements of the genetic architecture of autism and schizophrenia. © 2012 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 11/2012; · 3.23 Impact Factor
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    ABSTRACT: BACKGROUND: People usually feel they cause their own actions and the consequences of those actions, i.e., they attribute behavior to the proper agent. Research suggests that there are two routes to the experience of self-agency: 1) an explicit route, where one has the intention to obtain a goal (if it occurs, I must have done it) and 2) an implicit route, where information about the goal is unconsciously available and increases the feeling of self-agency. Schizophrenia patients typically experience no behavioral control and exhibit difficulties in distinguishing one's own actions from those of others. The present study investigates differences in both routes to self-agency experiences between schizophrenia patients and controls. METHODS: Twenty-three schizophrenia patients and 23 controls performed a task where they performed an action (button press) and subsequently indicated whether or not they were the agent of the consequence of this action (the outcome) on a 9-point scale. The task can be manipulated to measure both the explicit and implicit route (by using priming) to the experience of self-agency. RESULTS: In the explicit condition (participants intended to produce a specific outcome, and this outcome matched their goal), both groups experienced enhanced self-agency. In the implicit condition (the outcome matched the primed outcome), healthy controls showed increased self-agency over the outcome, while patients did not. Potential differences in task motivation and attention did not explain these findings. CONCLUSIONS: These findings provide new evidence for the idea that implicit processes leading to feelings of self-agency may be disturbed in schizophrenia.
    Schizophrenia Research 11/2012; · 4.59 Impact Factor
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    ABSTRACT: OBJECTIVE: To investigate whether advanced paternal age is associated with increased psychotic-like experiences (PLEs) and increased sensitivity to Cannabis in the offspring. METHODS: A cross-sectional population-based study in 1684 participants aged 18 to 25. RESULTS: We found no association of paternal age with PLEs. Only the positive dimension subscale was associated to paternal age, but that could be largely contributed to outliers. Also no increased sensitivity to Cannabis smoking was apparent. CONCLUSION: In the general population, we did not find robust support for an association between paternal age and vulnerability to PLEs in 18-25year old offspring.
    Schizophrenia Research 11/2012; · 4.59 Impact Factor
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    ABSTRACT: BACKGROUND: The predominant model for regulation of gene expression through DNA methylation is an inverse association in which increased methylation results in decreased gene expression levels. However, recent studies suggest that the relationship between genetic variation, DNA methylation and expression is more complex. RESULTS: Systems genetic approaches for examining relationships between gene expression and methylation array data were used to find both negative and positive associations between these levels. A weighted correlation network analysis reveals that i) both transcriptome and methylome are organized in modules, ii) co-expression modules are generally not preserved in the methylation data and vice-versa, and iii) highly significant correlations exist between co-expression and co-methylation modules, suggesting the existence of factors that affect expression and methylation of different modules (i.e., trans effects at the level of modules). We observed that methylation probes associated with expression in cis were more likely to be located outside CpG islands, whereas specificity for CpG island shores was present when methylation, associated with expression, was under local genetic control. A structural equation model based analysis found strong support in particular for a traditional causal model in which gene expression is regulated by genetic variation via DNA methylation instead of gene expression affecting DNA methylation levels. CONCLUSIONS: Our results provide new insights into the complex mechanisms between genetic markers, epigenetic mechanisms and gene expression. We find strong support for the classical model of genetic variants regulating methylation, which in turn regulates gene expression. Moreover we show that, although the methylation and expression modules differ, they are highly correlated.
    BMC Genomics 11/2012; 13(1):636. · 4.40 Impact Factor
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    ABSTRACT: PURPOSE: Both increased as well as decreased cancer mortality among psychiatric patients has been reported, but competing death causes were not included in the analyses. This study aims to investigate whether observed cancer mortality in patients with psychiatric disorders might be biased by competing death causes. METHOD: In this retrospective cohort study on data from the Psychiatric Case Register Middle Netherlands linked to the death register of Statistics Netherlands, the risk of cancer death among patients with schizophrenia (N = 4,590), bipolar disorder (N = 2,077), depression (N = 15,130) and their matched controls (N = 87,405) was analyzed using a competing risk model. RESULTS: Compared to controls, higher hazards of cancer death were found in patients with schizophrenia (HR = 1.61, 95 % CI 1.26-2.06), bipolar disorder (HR = 1.20, 95 % CI 0.81-1.79) and depression (HR = 1.26, 95 % CI 1.10-1.44). However, the HRs of death due to suicide and other death causes were more elevated. Consequently, among those who died, the 12-year cumulative risk of cancer death was significantly lower. CONCLUSIONS: Our analysis shows that, compared to the general population, psychiatric patients are at higher risk of dying from cancer, provided that they survive the much more elevated risks of suicide and other death causes.
    Social Psychiatry 10/2012; · 2.05 Impact Factor

Publication Stats

14k Citations
2,670.54 Total Impact Points

Institutions

  • 1998–2014
    • University Medical Center Utrecht
      • • Department of Psychiatry
      • • Department of Child and Adolescent Psychiatry
      • • Department of Neurosurgery
      Utrecht, Utrecht, Netherlands
    • Universiteit Utrecht
      • • Department of Psychiatry
      • • Division of Experimental Psychology
      Utrecht, Utrecht, Netherlands
  • 2010–2013
    • VU University Amsterdam
      • Department of Biological Psychology
      Amsterdam, North Holland, Netherlands
    • Heinrich-Heine-Universität Düsseldorf
      Düsseldorf, North Rhine-Westphalia, Germany
  • 2012
    • University of California, San Diego
      San Diego, California, United States
    • University of Malaya
      • Department of Psycological Medicine
      Kuala Lumpur, Kuala Lumpur, Malaysia
    • MRC Clinical Sciences Centre
      London Borough of Harrow, England, United Kingdom
    • Vanderbilt University
      Nashville, Michigan, United States
  • 2011–2012
    • Netherlands Institute for Neuroscience
      Amsterdamo, North Holland, Netherlands
    • Leiden University
      Leyden, South Holland, Netherlands
    • Parnassia Bavo Groep
      's-Gravenhage, South Holland, Netherlands
    • University of Zurich
      Zürich, Zurich, Switzerland
  • 2005–2012
    • Medizinische Universität Innsbruck
      • • Department für Psychiatrie und Psychotherapie
      • • Univ.-Klinik für Biologische Psychiatrie
      Innsbruck, Tyrol, Austria
  • 2002–2011
    • Academisch Medisch Centrum Universiteit van Amsterdam
      • • Department of Psychiatry
      • • Department of Social Medicine
      Amsterdam, North Holland, Netherlands
    • St. Elisabeth Ziekenhuis Tilburg
      Tilburg, North Brabant, Netherlands
  • 2009
    • University of Cape Town
      • Faculty of Health Sciences
      Cape Town, Province of the Western Cape, South Africa
    • Sheba Medical Center
      Gan, Tel Aviv, Israel
    • Universitair Medisch Centrum Groningen
      Groningen, Groningen, Netherlands
    • University of Copenhagen
      • Centre for Neuropsychiatric Schizophrenia Research
      Copenhagen, Capital Region, Denmark
  • 2006–2008
    • University of Groningen
      • NeuroImaging Center (NIC)
      Groningen, Province of Groningen, Netherlands
  • 2007
    • Hospital General Universitario Gregorio Marañón
      Madrid, Madrid, Spain
    • Lund University
      Lund, Skåne, Sweden
  • 1996
    • Nathan Kline Institute
      Orangeburg, New York, United States
  • 1991–1994
    • Mount Sinai School of Medicine
      • Department of Psychiatry
      Manhattan, NY, United States
    • Mount Sinai Medical Center
      New York City, New York, United States