Arthur W Toga

Keck School of Medicine USC, Los Ángeles, California, United States

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Publications (1000)4415.41 Total impact

  • Karen L Crawford, Scott C Neu, Arthur W Toga
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    ABSTRACT: The LONI Image and Data Archive (IDA)(1) is a repository for sharing and long-term preservation of neuroimaging and biomedical research data. Originally designed to archive strictly medical image files, the IDA has evolved over the last ten years and now encompasses the storage and dissemination of neuroimaging, clinical, biospecimen, and genetic data. In this article, we report upon the genesis of the IDA and how it currently securely manages data and protects data ownership. Copyright © 2015 Elsevier Inc. All rights reserved.
    NeuroImage 05/2015; DOI:10.1016/j.neuroimage.2015.04.067 · 6.13 Impact Factor
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    ABSTRACT: This article investigates subjects aged 55 to 65 from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database to broaden our understanding of early-onset (EO) cognitive impairment using neuroimaging and genetics biomarkers. Nine of the subjects had EO-AD (Alzheimer's disease) and 27 had EO-MCI (mild cognitive impairment). The 15 most important neuroimaging markers were extracted with the Global Shape Analysis (GSA) Pipeline workflow. The 20 most significant single nucleotide polymorphisms (SNPs) were chosen and were associated with specific neuroimaging biomarkers. We identified associations between the neuroimaging phenotypes and genotypes for a total of 36 subjects. Our results for all the subjects taken together showed the most significant associations between rs7718456 and L_hippocampus (volume), and between rs7718456 and R_hippocampus (volume). For the 27 MCI subjects, we found the most significant associations between rs6446443 and R_superior_frontal_gyrus (volume), and between rs17029131 and L_Precuneus (volume). For the nine AD subjects, we found the most significant associations between rs16964473 and L_rectus gyrus (surface area), and between rs12972537 and L_rectus_gyrus (surface area). We observed significant correlations between the SNPs and the neuroimaging phenotypes in the 36 EO subjects in terms of neuroimaging genetics. However, larger sample sizes are needed to ensure that the effects will be detectable for a reasonable false-positive error rate using the GSA and Plink Pipeline workflows.
    Psychiatry investigation 05/2015; 12(1):125-35. DOI:10.4306/pi.2015.12.1.125 · 1.15 Impact Factor
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    Naveen Ashish, Arthur W Toga
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    ABSTRACT: This paper presents a system for declaratively transforming medical subjects' data into a common data model representation. Our work is part of the "GAAIN" project on Alzheimer's disease data federation across multiple data providers. We present a general purpose data transformation system that we have developed by leveraging the existing state-of-the-art in data integration and query rewriting. In this work we have further extended the current technology with new formalisms that facilitate expressing a broader range of data transformation tasks, plus new execution methodologies to ensure efficient data transformation for disease datasets.
    Frontiers in Neuroinformatics 02/2015; 9:1. DOI:10.3389/fninf.2015.00001
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    Brain 02/2015; DOI:10.1093/brain/awv037 · 10.23 Impact Factor
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    ABSTRACT: Under the umbrella of the National Database for Clinical Trials (NDCT) related to mental illnesses, the National Database for Autism Research (NDAR) seeks to gather, curate, and make openly available neuroimaging data from NIH-funded studies of autism spectrum disorder (ASD). NDAR has recently made its database accessible through the LONI Pipeline workflow design and execution environment to enable large-scale analyses of cortical architecture and function via local, cluster, or "cloud"-based computing resources. This presents a unique opportunity to overcome many of the customary limitations to fostering biomedical neuroimaging as a science of discovery. Providing open access to primary neuroimaging data, workflow methods, and high-performance computing will increase uniformity in data collection protocols, encourage greater reliability of published data, results replication, and broaden the range of researchers now able to perform larger studies than ever before. To illustrate the use of NDAR and LONI Pipeline for performing several commonly performed neuroimaging processing steps and analyses, this paper presents example workflows useful for ASD neuroimaging researchers seeking to begin using this valuable combination of online data and computational resources. We discuss the utility of such database and workflow processing interactivity as a motivation for the sharing of additional primary data in ASD research and elsewhere.
    Brain Imaging and Behavior 02/2015; 9(1). DOI:10.1007/s11682-015-9354-z · 3.39 Impact Factor
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    ABSTRACT: The highly complex structure of the human brain is strongly shaped by genetic influences1. Subcortical brain regions form circuits with cortical areas to coordinate movement2, learning, memory3 and motivation4, and altered circuits can lead to abnormal behaviour and disease2. To investigate how common genetic variants affect the structure of these brain regions, here we conduct genome-wide association studies of the volumes of seven subcortical regions and the intracranial volume derived from magnetic resonance images of 30,717 individuals from 50 cohorts. We identify five novel genetic variants influencing the volumes of the putamen and caudate nucleus. We also find stronger evidence for three loci with previously established influences on hippocampal volume5 and intracranial volume6. These variants show specific volumetric effects on brain structures rather than global effects across structures. The strongest effects were found for the putamen, where a novel intergenic locus with replicable influence on volume (rs945270; P = 1.08 × 10−33; 0.52% variance explained) showed evidence of altering the expression of the KTN1 gene in both brain and blood tissue. Variants influencing putamen volume clustered near developmental genes that regulate apoptosis, axon guidance and vesicle transport. Identification of these genetic variants provides insight into the causes of variability in human brain development, and may help to determine mechanisms of neuropsychiatric dysfunction.
    Nature 01/2015; DOI:10.1038/nature14101 · 42.35 Impact Factor
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    ABSTRACT: The blood-brain barrier (BBB) limits entry of blood-derived products, pathogens, and cells into the brain that is essential for normal neuronal functioning and information processing. Post-mortem tissue analysis indicates BBB damage in Alzheimer's disease (AD). The timing of BBB breakdown remains, however, elusive. Using an advanced dynamic contrast-enhanced MRI protocol with high spatial and temporal resolutions to quantify regional BBB permeability in the living human brain, we show an age-dependent BBB breakdown in the hippocampus, a region critical for learning and memory that is affected early in AD. The BBB breakdown in the hippocampus and its CA1 and dentate gyrus subdivisions worsened with mild cognitive impairment that correlated with injury to BBB-associated pericytes, as shown by the cerebrospinal fluid analysis. Our data suggest that BBB breakdown is an early event in the aging human brain that begins in the hippocampus and may contribute to cognitive impairment. Copyright © 2015 Elsevier Inc. All rights reserved.
    Neuron 01/2015; 85(2):296-302. DOI:10.1016/j.neuron.2014.12.032 · 15.98 Impact Factor
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    ABSTRACT: The discovery of several genes that affect the risk for Alzheimer's disease ignited a worldwide search for single-nucleotide polymorphisms (SNPs), common genetic variants that affect the brain. Genome-wide search of all possible SNP-SNP interactions is challenging and rarely attempted because of the complexity of conducting approximately 1011 pairwise statistical tests. However, recent advances in machine learning, for example, iterative sure independence screening, make it possible to analyze data sets with vastly more predictors than observations. Using an implementation of the sure independence screening algorithm (called EPISIS), we performed a genome-wide interaction analysis testing all possible SNP-SNP interactions affecting regional brain volumes measured on magnetic resonance imaging and mapped using tensor-based morphometry. We identified a significant SNP-SNP interaction between rs1345203 and rs1213205 that explains 1.9% of the variance in temporal lobe volume. We mapped the whole brain, voxelwise effects of the interaction in the Alzheimer's Disease Neuroimaging Initiative data set and separately in an independent replication data set of healthy twins (Queensland Twin Imaging). Each additional loading in the interaction effect was associated with approximately 5% greater brain regional brain volume (a protective effect) in both Alzheimer's Disease Neuroimaging Initiative and Queensland Twin Imaging samples.
    Neurobiology of Aging 01/2015; 36:S151-S158. DOI:10.1016/j.neurobiolaging.2014.02.033 · 4.85 Impact Factor
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    ABSTRACT: Smaller hippocampal volume has been reported in individuals with post-traumatic stress disorder (PTSD) and dissociative identity disorder (DID), but the regional specificity of hippocampal volume reductions and the association with severity of dissociative symptoms and/or childhood traumatization are still unclear. Brain structural magnetic resonance imaging scans were analyzed for 33 outpatients (17 with DID and 16 with PTSD only) and 28 healthy controls (HC), all matched for age, sex, and education. DID patients met criteria for PTSD (PTSD-DID). Hippocampal global and subfield volumes and shape measurements were extracted. We found that global hippocampal volume was significantly smaller in all 33 patients (left: 6.75%; right: 8.33%) compared with HC. PTSD-DID (left: 10.19%; right: 11.37%) and PTSD-only with a history of childhood traumatization (left: 7.11%; right: 7.31%) had significantly smaller global hippocampal volume relative to HC. PTSD-DID had abnormal shape and significantly smaller volume in the CA2-3, CA4-DG and (pre)subiculum compared with HC. In the patient groups, smaller global and subfield hippocampal volumes significantly correlated with higher severity of childhood traumatization and dissociative symptoms. These findings support a childhood trauma-related etiology for abnormal hippocampal morphology in both PTSD and DID and can further the understanding of neurobiological mechanisms involved in these disorders. Hum Brain Mapp, 2014. © 2014 Wiley Periodicals, Inc. © 2014 Wiley Periodicals, Inc.
    Human Brain Mapping 12/2014; DOI:10.1002/hbm.22730 · 6.92 Impact Factor
  • Arthur W Toga, Paul M Thompson
    Brain 12/2014; 137(Pt 12):3104-6. DOI:10.1093/brain/awu276 · 10.23 Impact Factor
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    ABSTRACT: Memory impairment is the cardinal early feature of Alzheimer's disease, a highly prevalent disorder whose causes remain only partially understood. To identify novel genetic predictors, we used an integrative genomics approach to perform the largest study to date of human memory (n=14 781). Using a genome-wide screen, we discovered a novel association of a polymorphism in the pro-apoptotic gene FASTKD2 (fas-activated serine/threonine kinase domains 2; rs7594645-G) with better memory performance and replicated this finding in independent samples. Consistent with a neuroprotective effect, rs7594645-G carriers exhibited increased hippocampal volume and gray matter density and decreased cerebrospinal fluid levels of apoptotic mediators. The MTOR (mechanistic target of rapamycin) gene and pathways related to endocytosis, cholinergic neurotransmission, epidermal growth factor receptor signaling and immune regulation, among others, also displayed association with memory. These findings nominate FASTKD2 as a target for modulating neurodegeneration and suggest potential mechanisms for therapies to combat memory loss in normal cognitive aging and dementia.Molecular Psychiatry advance online publication 11 November 2014; doi:10.1038/mp.2014.142.
    Molecular Psychiatry 11/2014; DOI:10.1038/mp.2014.142 · 15.15 Impact Factor
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    ABSTRACT: Supernumerary sex chromosome aneuploidies (sSCA) are characterized by the presence of one or more additional sex chromosomes in an individual's karyotype; they affect around 1 in 400 individuals. Although there is high variability, each sSCA subtype has a characteristic set of cognitive and physical phenotypes. Here, we investigated the differences in the morphometry of the human corpus callosum (CC) between sex-matched controls 46,XY (N =99), 46,XX (N =93), and six unique sSCA karyotypes: 47,XYY (N =29), 47,XXY (N =58), 48,XXYY (N =20), 47,XXX (N =30), 48,XXXY (N =5), and 49,XXXXY (N =6). We investigated CC morphometry using local and global area, local curvature of the CC boundary, and between-landmark distance analysis (BLDA). We hypothesized that CC morphometry would vary differentially along a proposed spectrum of Y:X chromosome ratio with supernumerary Y karyotypes having the largest CC areas and supernumerary X karyotypes having significantly smaller CC areas. To investigate this, we defined an sSCA spectrum based on a descending Y:X karyotype ratio: 47,XYY, 46,XY, 48,XXYY, 47,XXY, 48,XXXY, 49,XXXXY, 46,XX, 47,XXX. We similarly explored the effects of both X and Y chromosome numbers within sex. Results of shape-based metrics were analyzed using permutation tests consisting of 5,000 iterations. Several subregional areas, local curvature, and BLDs differed between groups. Moderate associations were found between area and curvature in relation to the spectrum and X and Y chromosome counts. BLD was strongly associated with X chromosome count in both male and female groups. Our results suggest that X- and Y-linked genes have differential effects on CC morphometry. To our knowledge, this is the first study to compare CC morphometry across these extremely rare groups.
    10/2014; 5:16. DOI:10.1186/s13293-014-0016-4
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    ABSTRACT: A significant portion of our risk for dementia in old age is associated with lifestyle factors (diet, exercise, and cardiovascular health) that are modifiable, at least in principle. One such risk factor, high-homocysteine levels in the blood, is known to increase risk for Alzheimer's disease and vascular disorders. Here, we set out to understand how homocysteine levels relate to 3D surface-based maps of cortical gray matter distribution (thickness, volume, and surface area) computed from brain magnetic resonance imaging in 803 elderly subjects from the Alzheimer's Disease Neuroimaging Initiative data set. Individuals with higher plasma levels of homocysteine had lower gray matter thickness in bilateral frontal, parietal, occipital, and right temporal regions and lower gray matter volumes in left frontal, parietal, temporal, and occipital regions, after controlling for diagnosis, age, and sex and after correcting for multiple comparisons. No significant within-group associations were found in cognitively healthy people, patients with mild cognitive impairment, or patients with Alzheimer's disease. These regional differences in gray matter structure may be useful biomarkers to assess the effectiveness of interventions, such as vitamin B supplements, that aim to prevent homocysteine-related brain atrophy by normalizing homocysteine levels. Copyright © 2014 Elsevier Inc. All rights reserved.
    Neurobiology of Aging 08/2014; 36. DOI:10.1016/j.neurobiolaging.2014.01.154 · 4.85 Impact Factor
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    ABSTRACT: Alzheimer's disease (AD) is characterized by cortical atrophy and disrupted anatomic connectivity, and leads to abnormal interactions between neural systems. Diffusion-weighted imaging (DWI) and graph theory can be used to evaluate major brain networks and detect signs of a breakdown in network connectivity. In a longitudinal study using both DWI and standard magnetic resonance imaging (MRI), we assessed baseline white-matter connectivity patterns in 30 subjects with mild cognitive impairment (MCI, mean age 71.8 ± 7.5 years, 18 males and 12 females) from the Alzheimer's Disease Neuroimaging Initiative. Using both standard MRI-based cortical parcellations and whole-brain tractography, we computed baseline connectivity maps from which we calculated global "small-world" architecture measures, including mean clustering coefficient and characteristic path length. We evaluated whether these baseline network measures predicted future volumetric brain atrophy in MCI subjects, who are at risk for developing AD, as determined by 3-dimensional Jacobian "expansion factor maps" between baseline and 6-month follow-up anatomic scans. This study suggests that DWI-based network measures may be a novel predictor of AD progression. Copyright © 2014 Elsevier Inc. All rights reserved.
    Neurobiology of Aging 08/2014; 36. DOI:10.1016/j.neurobiolaging.2014.04.038 · 4.85 Impact Factor
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    ABSTRACT: Dynamic changes in the brain's lateral ventricles on magnetic resonance imaging are powerful biomarkers of disease progression in mild cognitive impairment (MCI) and Alzheimer's disease (AD). Ventricular measures can represent accumulation of diffuse brain atrophy with very high effect sizes. Despite having no direct role in cognition, ventricular expansion co-occurs with volumetric loss in gray and white matter structures. To better understand relationships between ventricular and cortical changes over time, we related ventricular expansion to atrophy in cognitively relevant cortical gray matter surfaces, which are more challenging to segment. In ADNI participants, percent change in ventricular volumes at 1-year (N = 677) and 2-year (N = 536) intervals was significantly associated with baseline cortical thickness and volume in the full sample controlling for age, sex, and diagnosis, and in MCI separately. Ventricular expansion in MCI was associated with thinner gray matter in frontal, temporal, and parietal regions affected by AD. Ventricular expansion reflects cortical atrophy in early AD, offering a useful biomarker for clinical trials of interventions to slow AD progression.
    Neurobiology of Aging 08/2014; 36. DOI:10.1016/j.neurobiolaging.2014.03.044 · 4.85 Impact Factor
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    ABSTRACT: We compare a variety of different anatomic connectivity measures, including several novel ones, that may help in distinguishing Alzheimer's disease (AD) patients from controls. We studied diffusion-weighted magnetic resonance imaging from 200 subjects scanned as part of the Alzheimer's Disease Neuroimaging Initiative. We first evaluated measures derived from connectivity matrices based on whole-brain tractography; next, we studied additional network measures based on a novel flow-based measure of brain connectivity, computed on a dense 3-dimensional lattice. Based on these 2 kinds of connectivity matrices, we computed a variety of network measures. We evaluated the measures' ability to discriminate disease with a repeated, stratified 10-fold cross-validated classifier, using support vector machines, a supervised learning algorithm. We tested the relative importance of different combinations of features based on the accuracy, sensitivity, specificity, and feature ranking of the classification of 200 people into normal healthy controls and people with early or late mild cognitive impairment or AD.
    Neurobiology of Aging 08/2014; 36. DOI:10.1016/j.neurobiolaging.2014.04.037 · 4.85 Impact Factor
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    ABSTRACT: In a previous report, we proposed a method for combining multiple markers of atrophy caused by Alzheimer's disease into a single atrophy score that is more powerful than any one feature. We applied the method to expansion rates of the lateral ventricles, achieving the most powerful ventricular atrophy measure to date. Here, we expand our method's application to tensor-based morphometry measures. We also combine the volumetric tensor-based morphometry measures with previously computed ventricular surface measures into a combined atrophy score. We show that our atrophy scores are longitudinally unbiased with the intercept bias estimated at 2 orders of magnitude below the mean atrophy of control subjects at 1 year. Both approaches yield the most powerful biomarker of atrophy not only for ventricular measures but also for all published unbiased imaging measures to date. A 2-year trial using our measures requires only 31 (22, 43) Alzheimer's disease subjects or 56 (44, 64) subjects with mild cognitive impairment to detect 25% slowing in atrophy with 80% power and 95% confidence.
    Neurobiology of Aging 08/2014; 36. DOI:10.1016/j.neurobiolaging.2014.05.038 · 4.85 Impact Factor
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    ABSTRACT: Brain connectivity is progressively disrupted in Alzheimer's disease (AD). Here, we used a seemingly unrelated regression (SUR) model to enhance the power to identify structural connections related to cognitive scores. We simultaneously solved regression equations with different predictors and used correlated errors among the equations to boost power for associations with brain networks. Connectivity maps were computed to represent the brain's fiber networks from diffusion-weighted magnetic resonance imaging scans of 200 subjects from the Alzheimer's Disease Neuroimaging Initiative. We first identified a pattern of brain connections related to clinical decline using standard regressions powered by this large sample size. As AD studies with a large number of diffusion tensor imaging scans are rare, it is important to detect effects in smaller samples using simultaneous regression modeling like SUR. Diagnosis of mild cognitive impairment or AD is well known to be associated with ApoE genotype and educational level. In a subsample with no apparent associations using the general linear model, power was boosted with our SUR model-combining genotype, educational level, and clinical diagnosis.
    Neurobiology of Aging 08/2014; 36. DOI:10.1016/j.neurobiolaging.2014.02.032 · 4.85 Impact Factor
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    ABSTRACT: Characterizing brain changes in Alzheimer's disease (AD) is important for patient prognosis and for assessing brain deterioration in clinical trials. In this diffusion weighted imaging study, we used a new fiber-tract modeling method to investigate white matter integrity in 50 elderly controls (CTL), 113 people with mild cognitive impairment, and 37 AD patients. After clustering tractography using a region-of-interest atlas, we used a shortest path graph search through each bundle's fiber density map to derive maximum density paths (MDPs), which we registered across subjects. We calculated the fractional anisotropy (FA) and mean diffusivity (MD) along all MDPs and found significant MD and FA differences between AD patients and CTL subjects, as well as MD differences between CTL and late mild cognitive impairment subjects. MD and FA were also associated with widely used clinical scores. As an MDP is a compact low-dimensional representation of white matter organization, we tested the utility of diffusion tensor imaging measures along these MDPs as features for support vector machine based classification of AD. Copyright © 2014. Published by Elsevier Inc.
    Neurobiology of Aging 08/2014; 36. DOI:10.1016/j.neurobiolaging.2014.05.037 · 4.85 Impact Factor
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    ABSTRACT: Developmental dyslexia is a common reading disorder that negatively impacts an individual's ability to achieve literacy. Although the brain network involved in reading and its dysfunction in dyslexia has been well studied, it is unknown whether dyslexia is caused by structural abnormalities in the reading network itself or in the lower-level networks that provide input to the reading network. In this study, we acquired structural magnetic resonance imaging scans longitudinally from 27 Norwegian children from before formal literacy training began until after dyslexia was diagnosed. Thus, we were able to determine that the primary neuroanatomical abnormalities that precede dyslexia are not in the reading network itself, but rather in lower-level areas responsible for auditory and visual processing and core executive functions. Abnormalities in the reading network itself were only observed at age 11, after children had learned how to read. The findings suggest that abnormalities in the reading network are the consequence of having different reading experiences, rather than dyslexia per se, whereas the neuroanatomical precursors are predominantly in primary sensory cortices.
    Brain 08/2014; 137(12). DOI:10.1093/brain/awu229 · 10.23 Impact Factor

Publication Stats

44k Citations
4,415.41 Total Impact Points


  • 2014–2015
    • Keck School of Medicine USC
      Los Ángeles, California, United States
  • 2007–2015
    • University of Southern California
      • • Department of Neurology
      • • Institute for Neuroimaging and Informatics (INI)
      • • Department of Psychology
      Los Ángeles, California, United States
    • University of California, San Francisco
      San Francisco, California, United States
    • University of Queensland
      Brisbane, Queensland, Australia
  • 2007–2014
    • CSU Mentor
      • Department of Neurology
      Long Beach, California, United States
  • 1989–2014
    • University of California, Los Angeles
      • • Department of Neurology
      • • Laboratory of Neuro Imaging
      • • Department of Medicine
      • • Department of Neurosurgery
      Los Angeles, California, United States
    • Columbia University
      • College of Physicians and Surgeons
      New York City, New York, United States
  • 2013
    • New Jersey Institute of Technology
      Newark, New Jersey, United States
  • 1988–2013
    • Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
      • Department of Medicine
      Torrance, California, United States
  • 2012
    • University of California, Irvine
      • Department of Psychiatry & Human Behavior
      Irvine, California, United States
  • 2006–2011
    • Johns Hopkins University
      • Department of Neurology
      Baltimore, Maryland, United States
    • Lawrence Livermore National Laboratory
      Livermore, California, United States
    • University of Zurich
      • Division of Neuropsychology
      Zürich, Zurich, Switzerland
  • 2009
    • University of Iowa
      • Department of Psychiatry
      Iowa City, Iowa, United States
  • 2004–2008
    • Università degli Studi di Brescia
      Brescia, Lombardy, Italy
    • University of Virginia
      • Department of Neurosurgery
      Charlottesville, Virginia, United States
  • 1996–2008
    • McGill University
      • • McConnell Brain Imaging Centre
      • • Montreal Neurological Institute
      Montréal, Quebec, Canada
  • 2006–2007
    • University of Pittsburgh
      • Department of Psychiatry
      Pittsburgh, Pennsylvania, United States
    • University of California, Davis
      • • Center for Neuroscience
      • • Department of Neurology
      Davis, CA, United States
  • 2001–2006
    • National Institute of Mental Health (NIMH)
      • Child Psychiatry Branch
      Maryland, United States
  • 2005
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1999–2005
    • Pacific Neuropsychiatric Institute
      Seattle, Washington, United States
  • 2003
    • University of Melbourne
      Melbourne, Victoria, Australia
    • University of Nice-Sophia Antipolis
      Nice, Provence-Alpes-Côte d'Azur, France
    • Otto-von-Guericke-Universität Magdeburg
      Magdeburg, Saxony-Anhalt, Germany
    • Humboldt-Universität zu Berlin
      Berlín, Berlin, Germany
  • 2001–2002
    • University of California, San Diego
      • Department of Psychiatry
      San Diego, California, United States
  • 1980–1987
    • Washington University in St. Louis
      • Department of Neurology
      San Luis, Missouri, United States
  • 1979
    • Saint Louis University
      • Division of Nephrology
      Saint Louis, Michigan, United States