Stephen V Faraone

CNS, Sydney, New South Wales, Australia

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Publications (988)5158.45 Total impact

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    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD) are highly comorbid disorders. ADHD has been associated with altered white matter (WM) microstructure, though the literature is inconsistent, which may be due to differences in the in- or exclusion of participants with comorbid ODD. WM abnormalities in ODD are still poorly understood, and it is unclear whether comorbid ODD in ADHD may have confounded the current ADHD literature. Diffusion Tensor Imaging (DTI) was used to compare fractional anisotropy (FA) and mean diffusivity (MD) between ADHD patients with (n = 42) and without (n = 117) comorbid ODD. All participants were between 8-25 years and groups did not differ in mean age or gender. Follow-up analyses were conducted to examine the role of antisocial behaviour (conduct problems) on FA and MD values in both groups. Comorbid ODD in ADHD was associated with lower FA in left frontotemporal WM, which appeared independent of ADHD symptoms. FA was negatively associated with antisocial behaviour in ADHD + ODD, but not in ADHD-only. Comorbid ODD is associated with WM abnormalities in individuals with ADHD, which appears to be independent of ADHD symptoms. Altered WM microstructure in comorbid ODD may play a role in inconsistencies in the current DTI literature in ADHD. Altered development of these tracts may contribute to social-emotional and cognitive problems in children with oppositional and antisocial behaviour.
    European Child & Adolescent Psychiatry 10/2015; DOI:10.1007/s00787-015-0784-3 · 3.34 Impact Factor
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    ABSTRACT: Objective: Oppositional Defiant Disorder (ODD) is highly prevalent in Attention-Deficit/Hyperactivity Disorder (ADHD) and may account for inconsistencies in findings on neurocognitive functioning in ADHD. Our aim was to assess cool and hot executive functioning (EF) and temporal processing in ADHD with and without comorbid ODD to elucidate the effects of comorbid ODD. Method: ADHD-only (n = 82), ADHD + ODD (n = 82), and controls (n = 82), with mean age 16 years (SD = 3.1), matched for age, gender, IQ, and ADHD type (clinical groups) were assessed on cool EF (inhibition, working memory), hot EF (reinforcement processing, emotion recognition), and temporal processing (time production and reproduction). Results: Individuals with ADHD + ODD showed abnormalities in inhibition, working memory, facial emotion recognition, and temporal processing, whereas individuals with ADHD-only were solely impaired in working memory and time production. Conclusion: Findings suggest that ODD carries a substantial part of the EF deficits observed in ADHD and contrast with current theories of neurocognitive impairments in ADHD.
    Journal of Attention Disorders 10/2015; DOI:10.1177/1087054715606216 · 3.78 Impact Factor
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    ABSTRACT: A recent meta-analysis documented a significant statistical association between mild traumatic brain injury (mTBI) and attention deficit hyperactivity disorder (ADHD) (Adeyemo et al., 2014), but the direction of this effect was unclear. In this study, we hypothesized that ADHD would be an antecedent risk factor for mTBI. Participants were student athletes ages 12 to 25 who had sustained a mTBI and Controls of similar age and sex selected from studies of youth with and without ADHD. Subjects were assessed for symptoms of ADHD, concussion severity, and cognitive function. mTBI subjects had a significantly higher rate of ADHD than Controls, and in all cases the age of onset of ADHD was before mTBI onset. mTBI+ADHD subjects also had more severe concussion symptoms (fatigue and poor concentration) than mTBI-ADHD subjects. These results support ADHD as an antecedent risk factor for mTBI in student athletes and that its presence complicates the course of mTBI.
    The Journal of nervous and mental disease 10/2015; DOI:10.1097/NMD.0000000000000375 · 1.69 Impact Factor

  • Third International Congress on ADHD, Berlin, Germany; 10/2015
  • Mai Uchida · Thomas J Spencer · Stephen V Faraone · Joseph Biederman ·
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    ABSTRACT: Objective: We aimed to provide an overview of the Massachusetts General Hospital (MGH) Longitudinal Studies of ADHD. Methods: We evaluated and followed samples of boys and girls with and without ADHD ascertained from psychiatric and pediatric sources and their families. Results: These studies documented that ADHD in both sexes is associated with high levels of persistence into adulthood, high levels of familiality with ADHD and other psychiatric disorders, a wide range of comorbid psychiatric and cognitive disorders including mood, anxiety, and substance use disorders, learning disabilities, executive function deficits, emotional dysregulation, and autistic traits as well as functional impairments. The MGH studies suggested that stimulant treatment decreased risks of developing comorbid psychiatric disorders, substance use disorders, and functional outcomes. The MGH studies documented the neural basis of persistence of ADHD using neuroimaging. Conclusion: The MGH studies provided various insights on symptoms, course, functions, comorbidities, and neuroscience of ADHD.
    Journal of Attention Disorders 09/2015; DOI:10.1177/1087054715604360 · 3.78 Impact Factor
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    ABSTRACT: We recently described a hemi-deletion on chromosome 9p24.2 at the SLC1A1 gene lcous and its co-segregation with schizophrenia in an extended Palauan pedigree. This finding represents a point of convergence for several pathophysiological models of schizophrenia. The present report sought to characterize the biological consequences of this hemi-deletion. Dual luciferase assays demonstrated that the partially-deleted allele (lacking exon 1 and the native promoter) can drive expression of a 5'-truncated SLC1A1 using sequence upstream of exon 2 as a surrogate promoter. However, confocal microscopy and electrophysiological recordings demonstrate that the 5'-truncated SLC1A1 lacks normal membrane localization and glutamate transport ability. To identify downstream consequences of the hemi-deletion we first used a themed qRT-PCR array to compare expression of 84 GABA and glutamate genes in RNA from peripheral blood leukocytes in deletion carriers (n=11) vs. non-carriers (n=8) as well as deletion carriers with psychosis (n=5) vs. those without (n=3). Then, targeted RNA-Seq (TREx) was used to quantify expression of 375 genes associated with neuropsychiatric disorders in HEK293 cells subjected to either knockdown of SLC1A1 or overexpression of full-length or 5'-truncated SLC1A1. Expression changes of several genes strongly implicated in schizophrenia pathophysiology were detected (e.g., SLC1A2, SLC1A3, SLC1A6, SLC7A11, GRIN2A, GRIA1, DLX1).
    09/2015; 1(3):125-144. DOI:10.1159/000433599
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    ABSTRACT: The Research Domain Criteria (RDoC) address three types of aggression: frustrative non-reward, defensive aggression and offensive/proactive aggression. This review sought to present the evidence for genetic underpinnings of aggression and to determine to what degree prior studies have examined phenotypes that fit into the RDoC framework. Although the constructs of defensive and offensive aggression have been widely used in the animal genetics literature, the human literature is mostly agnostic with regard to all the RDoC constructs. We know from twin studies that about half the variance in behavior may be explained by genetic risk factors. This is true for both dimensional, trait-like, measures of aggression and categorical definitions of psychopathology. The non-shared environment seems to have a moderate influence with the effects of shared environment being unclear. Human molecular genetic studies of aggression are in an early stage. The most promising candidates are in the dopaminergic and serotonergic systems along with hormonal regulators. Genome-wide association studies have not yet achieved genome-wide significance, but current samples are too small to detect variants having the small effects one would expect for a complex disorder. The strongest molecular evidence for a genetic basis for aggression comes from animal models comparing aggressive and non-aggressive strains or documenting the effects of gene knockouts. Although we have learned much from these prior studies, future studies should improve the measurement of aggression by using a systematic method of measurement such as that proposed by the RDoC initiative. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 09/2015; DOI:10.1002/ajmg.b.32364 · 3.42 Impact Factor
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    ABSTRACT: In 2009, the U.S. National Institute of Mental Health (NIMH) proposed an approach toward the deconstruction of psychiatric nosology under the research domain criteria (RDoC) framework. The overarching goal of RDoC is to identify robust, objective measures of behavior, emotion, cognition, and other domains that are more closely related to neurobiology than are diagnoses. A preliminary framework has been constructed, which has connected molecules, genes, brain circuits, behaviors, and other elements to dimensional psychiatric constructs. Although the RDoC framework has salience in emerging studies, foundational literature that pre-dated this framework requires synthesis and translation to the evolving objectives and nomenclature of RDoC. Toward this end, we review the candidate-gene association, linkage, and genome-wide studies that have implicated a variety of loci and genetic polymorphisms in selected Positive Valence Systems (PVS) constructs. Our goal is to review supporting evidence to currently listed genes implicated in this domain and novel candidates. We systematically searched and reviewed literature based on keywords listed under the June, 2011, edition of the PVS matrix on the RDoC website (, which were supplemented with de novo keywords pertinent to the scope of our review. Several candidate genes linked to the PVS framework were identified from candidate-gene association studies. We also identified novel candidates with loose association to PVS traits from genome-wide studies. There is strong evidence suggesting that PVS constructs, as currently conceptualized under the RDoC initiative, index genetically influenced traits; however, future research, including genetic epidemiological, and psychometric analyses, must be performed. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 09/2015; DOI:10.1002/ajmg.b.32382 · 3.42 Impact Factor
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    ABSTRACT: Background Evidence that different neuropsychiatric conditions share genetic liability has increased interest in phenotypes with ‘cross-disorder’ relevance, as they may contribute to revised models of psychopathology. Cognition is a promising construct for study; yet, evidence that the same cognitive functions are impaired across different forms of psychopathology comes primarily from separate studies of individual categorical diagnoses versus controls. Given growing support for dimensional models that cut across traditional diagnostic boundaries, we aimed to determine, within a single cohort, whether performance on measures of executive functions (EFs) predicted dimensions of different psychopathological conditions known to share genetic liability.Methods Data are from 393 participants, ages 8–17, consecutively enrolled in the Longitudinal Study of Genetic Influences on Cognition (LOGIC). This project is conducting deep phenotyping and genomic analyses in youth referred for neuropsychiatric evaluation. Using structural equation modeling, we examined whether EFs predicted variation in core dimensions of the autism spectrum disorder, bipolar illness, and schizophrenia (including social responsiveness, mania/emotion regulation, and positive symptoms of psychosis, respectively).ResultsWe modeled three cognitive factors (working memory, shifting, and executive processing speed) that loaded on a second-order EF factor. The EF factor predicted variation in our three target traits, but not in a negative control (somatization). Moreover, this EF factor was primarily associated with the overlapping (rather than unique) variance across the three outcome measures, suggesting that it related to a general increase in psychopathology symptoms across those dimensions.Conclusions Findings extend support for the relevance of cognition to neuropsychiatric conditions that share underlying genetic risk. They suggest that higher-order cognition, including EFs, relates to the dimensional spectrum of each of these disorders and not just the clinical diagnoses. Moreover, results have implications for bottom-up models linking genes, cognition, and a general psychopathology liability.
    Journal of Child Psychology and Psychiatry 09/2015; DOI:10.1111/jcpp.12463 · 6.46 Impact Factor
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    ABSTRACT: Impulsivity and inattention related to attention deficit hyperactivity disorder (ADHD) may increase food intake and, consequently, weight gain. However, findings on the association between obesity/overweight and ADHD are mixed. The authors conducted a meta-analysis to estimate this association. A broad range of databases was searched through Aug. 31, 2014. Unpublished studies were also obtained. Study quality was rated with the Newcastle-Ottawa Scale. Random-effects models were used. Forty-two studies that included a total of 728,136 individuals (48,161 ADHD subjects; 679,975 comparison subjects) were retained. A significant association between obesity and ADHD was found for both children (odds ratio=1.20, 95% CI=1.05-1.37) and adults (odds ratio=1.55, 95% CI=1.32-1.81). The pooled prevalence of obesity was increased by about 70% in adults with ADHD (28.2%, 95% CI=22.8-34.4) compared with those without ADHD (16.4%, 95% CI=13.4-19.9), and by about 40% in children with ADHD (10.3%, 95% CI=7.9-13.3) compared with those without ADHD (7.4%, 95% CI=5.4-10.1). The significant association between ADHD and obesity remained when limited to studies 1) reporting odds ratios adjusted for possible confounding factors; 2) diagnosing ADHD by direct interview; and 3) using directly measured height and weight. Gender, study setting, study country, and study quality did not moderate the association between obesity and ADHD. ADHD was also significantly associated with overweight. Individuals medicated for ADHD were not at higher risk of obesity. This study provides meta-analytic evidence for a significant association between ADHD and obesity/overweight. Further research should address possible underlying mechanisms and the long-term effects of ADHD treatments on weight in individuals with both ADHD and obesity.
    American Journal of Psychiatry 08/2015; DOI:10.1176/appi.ajp.2015.15020266 · 12.30 Impact Factor
  • Yanli Zhang-James · Stephen V Faraone ·
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    ABSTRACT: Genetic studies of human aggression have mainly focused on known candidate genes and pathways regulating serotonin and dopamine signaling and hormonal functions. These studies have taught us much about the genetics of human aggression, but no genetic locus has yet achieved genome-significance. We here present a review based on a paradoxical hypothesis that studies of rare, functional genetic variations can lead to a better understanding of the molecular mechanisms underlying complex multifactorial disorders such as aggression. We examined all aggression phenotypes catalogued in Online Mendelian Inheritance in Man (OMIM), an Online Catalog of Human Genes and Genetic Disorders. We identified 95 human disorders that have documented aggressive symptoms in at least one individual with a well-defined genetic variant. Altogether, we retrieved 86 causal genes. Although most of these genes had not been implicated in human aggression by previous studies, the most significantly enriched canonical pathways had been previously implicated in aggression (e.g., serotonin and dopamine signaling). Our findings provide strong evidence to support the causal role of these pathways in the pathogenesis of aggression. In addition, the novel genes and pathways we identified suggest additional mechanisms underlying the origins of human aggression. Genome-wide association studies with very large samples will be needed to determine if common variants in these genes are risk factors for aggression. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 08/2015; DOI:10.1002/ajmg.b.32363 · 3.42 Impact Factor
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    ABSTRACT: Recently, numerous genome-wide association studies (GWASs) have identified numerous risk loci for schizophrenia, but follow-up studies are still essential to confirm those results. Therefore, we followed up on top GWAS hits by genotyping implicated loci in additional schizophrenia family samples from our own collection. Five-hundred thirty-six Asian families (comprising 1633 members including 698 schizophrenics) were genotyped in this study. We analyzed 12 single nucleotide polymorphisms (SNPs) in strongly implicated candidate genes revealed by GWASs and their follow-up studies. We then used meta-analysis to combine our results with those of the Schizophrenia Working Group of the Psychiatric Genomics Consortium (PGC). In our newly genotyped samples, there were no significant associations of any of the 12 candidate SNPs with schizophrenia; however, all genome-wide significant results from the schizophrenia PGC analysis were maintained after combination with our new data by meta-analysis. One SNP (rs4765905 in CACNA1C) showed a stronger effect and decreased p-value (5.14e-17) after meta-analysis relative to the original PGC results, with no significant between-study heterogeneity. The findings of this study support the significant results in the PGC, especially for CACNA1C. The sample size in our study was considerably smaller than that in the PGC-SCZ study; thus, the weights carried by our samples in the meta-analysis were small. Therefore, our data could not vastly reduce PGC association signals. However, we considered that the well replicated results from the PGC hold up in our new samples, and may suggest that the top hits from the PGC are generalizable, even to other ancestral groups. Copyright © 2015 Elsevier B.V. All rights reserved.
    Schizophrenia Research 08/2015; 168(1). DOI:10.1016/j.schres.2015.07.033 · 3.92 Impact Factor

  • 08/2015; DOI:10.1038/nrdp.2015.20
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    ABSTRACT: Children with deficits in emotional regulation operationalized by scores on the Child Behavior Checklist (CBCL) Attention Problems, Aggressive Behavior, and Anxious-Depressed subscales are more likely than others to manifest adverse outcomes. However, the transmission of this profile has not been well studied. The main aim of this study was to investigate the familiality of this profile. Participants were youth probands with bipolar I (BP-I) disorder (N = 140), ADHD (N = 83), and controls (N = 117) and their siblings. Based on the CBCL emotional dysregulation profile, we classified children with severe emotional dysregulation (aggregate cut-off score ≥210) and emotional dysregulation (aggregate cut-off score ≥ 180 and <210). Emotional dysregulation profile scores correlated positively between probands and siblings. Youth with emotional dysregulation are at increased risk to have siblings with similar deficits, suggesting that emotional dysregulation runs in families. © 2015 SAGE Publications.
    Journal of Attention Disorders 07/2015; DOI:10.1177/1087054715596576 · 3.78 Impact Factor
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    Marsha Kaitz · David Mankuta · Ann Marie Rokem · Stephen V Faraone ·
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    ABSTRACT: To test for gender-differences in the relation between mothers' antenatal anxiety and infants' body weight during gestation, at birth, and at 1-month of age. Two hundred and twelve randomly-recruited women were divided into two groups: Controls (n=105) and Anxious Group (n=107) based on a standard cut-off of the Beck Anxiety Inventory. Outcome measures were Fetal Weight derived from biometrics obtained from an ultrasound scan in the 3rd trimester and infants' weight at birth and at 1-month of age, both obtained from medical records. Multivariate analyses showed main effects of Gender on infants' birth weight (P=.001) and on infants' weight at 1-month of age (P=.004), but no main effects of Anxiety Group at any time-point. Gender x Anxiety Group interactions at all three time points (Fetal weight: P=.05; Birth weight: P=.03; 1-month of age: P=.10) reflected gender differences (males>females) among infants in the anxious group, but not among controls. Distinct trends regarding same sex comparisons across groups (Control vs. Anxiety) were in line with predictions (male controls<male anxious; female controls>females anxious). Controlling for Postpartum Anxiety and Antenatal and Postpartum Depression in the models did not affect primary results. Gender differences in fetal and birth weight were more substantial among infants of anxious mothers than among controls due to the seemingly accelerated growth of "anxious" males and the diminution of weight among "anxious" females. Copyright © 2015 Elsevier Inc. All rights reserved.
    Journal of psychosomatic research 07/2015; DOI:10.1016/j.jpsychores.2015.07.006 · 2.74 Impact Factor
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    ABSTRACT: Oppositional defiant disorder (ODD) is a frequent psychiatric disorder seen in children and adolescents with attention-deficit-hyperactivity disorder (ADHD). ODD is also a common antecedent to both affective disorders and aggressive behaviors. Although the heritability of ODD has been estimated to be around 0.60, there has been little research into the molecular genetics of ODD. The present study examined the association of irritable and defiant/vindictive dimensions and categorical subtypes of ODD (based on latent class analyses) with previously described specific polymorphisms (DRD4 exon3 VNTR, 5-HTTLPR, and seven OXTR SNPs) as well as with dopamine, serotonin, and oxytocin genes and pathways in a clinical sample of children and adolescents with ADHD. In addition, we performed a multivariate genome-wide association study (GWAS) of the aforementioned ODD dimensions and subtypes. Apart from adjusting the analyses for age and sex, we controlled for “parental ability to cope with disruptive behavior.” None of the hypothesis-driven analyses revealed a significant association with ODD dimensions and subtypes. Inadequate parenting behavior was significantly associated with all ODD dimensions and subtypes, most strongly with defiant/vindictive behaviors. In addition, the GWAS did not result in genome-wide significant findings but bioinformatics and literature analyses revealed that the proteins encoded by 28 of the 53 top-ranked genes functionally interact in a molecular landscape centered around Beta-catenin signaling and involved in the regulation of neurite outgrowth. Our findings provide new insights into the molecular basis of ODD and inform future genetic studies of oppositional behavior.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 07/2015; DOI:10.1002/ajmg.b.32346 · 3.42 Impact Factor
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    ABSTRACT: The Harvard Adolescent Family High Risk (FHR) Study examined multiple domains of function in young relatives of individuals diagnosed with schizophrenia to identify precursors of the illness. One such area is motor performance, which is deviant in people with schizophrenia and in children at risk for schizophrenia, usually offspring. The present study assessed accuracy of motor performance and degree of lateralization in FHR adolescents and young adults. Subjects were 33 non-psychotic, first-degree relatives of individuals diagnosed with schizophrenia, and 30 non-psychotic comparison subjects (NpC), ranging in age from 13 to 25 who were compared using a line-drawing task. FHR individuals exhibited less precise and coordinated line drawing but greater degree of lateralization than controls. Performance on the linedrawing task was correlated with degree of genetic loading, a possible predictor of higher risk for schizophrenia in the pedigree. The observation of increased motor deviance and increased lateralization in FHR can be utilized in identification and initiation of the treatment in those at high risk in order to prevent or delay the full manifestation of this devastating condition. The use of a rigorously quantified measure is likely to add to the sensitivity of measuring motor performance, especially when impairments may be subtle. Copyright © 2015 Elsevier B.V. All rights reserved.
    Schizophrenia Research 07/2015; 168(1). DOI:10.1016/j.schres.2015.06.013 · 3.92 Impact Factor

Publication Stats

58k Citations
5,158.45 Total Impact Points


  • 2015
    • CNS
      Sydney, New South Wales, Australia
  • 2012-2015
    • University of Bergen
      • Department of Biomedicine
      Bergen, Hordaland, Norway
    • University of South Wales
      Понтиприте, Wales, United Kingdom
    • Ghent University
      • Department of Experimental Clinical and Health Psychology
      Gand, Flanders, Belgium
  • 2005-2015
    • State University of New York Upstate Medical University
      • • Department of Neuroscience and Physiology
      • • Department of Psychiatry and Behavioral Sciences
      Syracuse, New York, United States
    • New York University
      New York City, New York, United States
    • Western Psychiatric Institute and Clinic
      Pittsburgh, Pennsylvania, United States
    • University of California, San Diego
      • Department of Psychiatry
      San Diego, CA, United States
  • 1991-2015
    • Massachusetts General Hospital
      • Department of Psychiatry
      Boston, Massachusetts, United States
  • 2014
    • Trinity College Dublin
      • Department of Psychiatry
      Dublin, Leinster, Ireland
    • Duke University Medical Center
      • Department of Medicine
      Durham, North Carolina, United States
    • King's College London
      Londinium, England, United Kingdom
  • 2013
    • VU University Amsterdam
      • Department of Clinical Neuropsychology
      Amsterdam, North Holland, Netherlands
  • 1989-2013
    • Harvard University
      • Social Neuroscience and Psychopathology Laboratory
      Cambridge, Massachusetts, United States
  • 2011
    • Hôpital Universitaire Robert Debré
      Lutetia Parisorum, Île-de-France, France
    • National Cheng Kung University
      • Institute of Clinical Medicine
      Tainan, Taiwan, Taiwan
    • University of Nebraska Medical Center
      Omaha, Nebraska, United States
  • 1985-2011
    • Harvard Medical School
      • • Department of Psychiatry
      • • Commonwealth Research Center
      Boston, Massachusetts, United States
  • 2009
    • University of California, Los Angeles
      Los Angeles, California, United States
  • 2008
    • Hospital Universitari i Politècnic la Fe
      Valenza, Valencia, Spain
  • 2007
    • Syracuse VA Medical Center
      Syracuse, New York, United States
    • Michigan State University
      • Department of Psychology
      East Lansing, MI, United States
  • 2006
    • University of Vermont
      • Department of Psychiatry
      Burlington, Vermont, United States
    • Beth Israel Deaconess Medical Center
      • Department of Psychiatry
      Boston, Massachusetts, United States
    • National Taiwan University Hospital
      • Department of Psychiatry
      Taipei, Taipei, Taiwan
  • 2004
    • Peking University
      • Institute of Mental Health
      Beijing, Beijing Shi, China
  • 2003
    • Yale University
      • Department of Psychiatry
      New Haven, Connecticut, United States
    • University of Utah
      • Department of Psychiatry
      Salt Lake City, Utah, United States
    • California State University, Sacramento
      Sacramento, California, United States
  • 2002
    • University of Haifa
      • Department of Psychology
      H̱efa, Haifa, Israel
    • University of Massachusetts Boston
      • Department of Psychology
      Boston, MA, United States
    • Tufts University
      • Department of Pediatrics
      Бостон, Georgia, United States
    • Tulane University
      New Orleans, Louisiana, United States
    • University of Pennsylvania
      • Department of Psychiatry
      Filadelfia, Pennsylvania, United States
  • 1989-2002
    • Boston University
      • Department of Psychology
      Boston, Massachusetts, United States
  • 2001
    • University of Washington Seattle
      • Department of Psychiatry and Behavioral Sciences
      Seattle, WA, United States
  • 2000
    • University of California, Davis
      • School of Medicine
      Davis, CA, United States
  • 1995
    • Beverly Hospital, Boston MA
      BVY, Massachusetts, United States
  • 1987
    • U.S. Food and Drug Administration
      Washington, Washington, D.C., United States