Michele T Pato

University of Southern California, Los Ángeles, California, United States

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Publications (99)522.99 Total impact

  • The American Journal of Human Genetics 10/2015; 97(4):576-592. DOI:10.1016/j.ajhg.2015.09.001 · 10.93 Impact Factor
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    ABSTRACT: Objectives: 1) To investigate the symptom dimensions of Schizophrenia using factor analyses (FA) of lifetime symptoms of a sample of Portuguese patients with diagnosis of Schizophrenia; 2) To analyze which symptom dimensions are significant predictors of clinical and demographic variables. Methodology: FA of the OPCRIT items (42 signs and symptoms) of 506 Schizophrenia patients assessed with the Diagnostic Interview for Genetic Studies. Only the items occurring in at least 10% of patients were included. Spearmen correlations were performed first, in order to select the potential dependent variables (demographic and clinical) to be included in the linear regression/logistic binary regression models to obtain Beta values/Odds-Ratio (OR). Results: 1. Following the Kaiser and the Cattel's Scree Plot criteria, a three-factor structure was selected, with an explained variance (EV) of 40.28%. Based on items content, the meaningful three factors were denominated F1 Depression (EV 6.64%; α=.91); F2 Positive symptoms (5.73%; α=.86); F3 Disorganization and Negative symptoms (4.54%; α=.84). 2. Age of onset (Beta=-.166) and Mode of onset (-.127) were predicted by F3; Course of disorder by F1 (-.105), F2 (-.140) and F3 (.403) and Deterioration only by F3 (1.596); Being single by F1 (OR .966) and F3 (1.081); Poor premorbid work (.902) and Social (.928) adjustment by F2 and Premorbid personality disorder by F1 (1.064); Family history of Schizophrenia by F3 (.919); Lifetime diagnosis of alcohol abuse/dependence (1.036) and of Other drug than cannabis (1.082) by F1 and F2, respectively; Alcohol (1.070) and Other drug than cannabis (1.084) abuse/dependence with psychopathology by F1 and F2, respectively. Also Cannabis abuse/dependence with psychopathology was explained by F2 (1.066) (all p<.005). Conclusions: This factorial structure is in accordance with other reports. Encompassing an approach based on individual clinical features and quantitative traits these results contribute to a better phenotypic refinement of schizophrenia.
    European Archives of Psychiatry and Clinical Neuroscience; 09/2015
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    ABSTRACT: Study Objectives To examine the association between substance use and short sleep duration in individuals with schizophrenia or schizoaffective disorder, depressive type (SADD).DesignCross-sectional, retrospective study.SettingUrban, suburban, and rural centers across the United States.Participants2,462 consented, adult individuals with schizophrenia or schizoaffective disorder, depressive type (SADD). Participants included inpatients in acute or chronic care settings as well as outpatients and residents in community dwellings.MeasurementsSubstance use was assessed with 10 questions adopted from well-validated measures (e.g., CAGE questionnaire) for alcohol, marijuana, and illicit drugs. Short sleep duration was defined as <6 hr of self-reported sleep per night.ResultsClose to 100% of our sample used nicotine while 83% used substances other than nicotine. More importantly, there was a significant association between substance use and short sleep duration. Interestingly, this association was strongest among African–Americans with schizophrenia or SADD.Conclusions Because psychiatric medications often target chemical receptors involved with both sleep and substance use, understanding the association between short sleep duration and substance use in individuals with schizophrenia and SADD is important. Given that the majority of premature deaths in individuals with psychotic illness are due to medical conditions associated with modifiable risk factors, prospective studies designed to examine the effect of short sleep duration on behaviors like substance use should be undertaken. Finally, analyzing genetic and environmental data in a future study might help illuminate the strong association found between short sleep duration and substance use in African–Americans with schizophrenia and SADD. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 09/2015; DOI:10.1002/ajmg.b.32374 · 3.42 Impact Factor
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    ABSTRACT: A long-standing epidemiological puzzle is the reduced rate of rheumatoid arthritis (RA) in those with schizophrenia (SZ) and vice versa. Traditional epidemiological approaches to determine if this negative association is underpinned by genetic factors would test for reduced rates of one disorder in relatives of the other, but sufficiently powered data sets are difficult to achieve. The genomics era presents an alternative paradigm for investigating the genetic relationship between two uncommon disorders. We use genome-wide common single nucleotide polymorphism (SNP) data from independently collected SZ and RA case-control cohorts to estimate the SNP correlation between the disorders. We test a genotype X environment (GxE) hypothesis for SZ with environment defined as winter- vs summer-born. We estimate a small but significant negative SNP-genetic correlation between SZ and RA (-0.046, s.e. 0.026, P = 0.036). The negative correlation was stronger for the SNP set attributed to coding or regulatory regions (-0.174, s.e. 0.071, P = 0.0075). Our analyses led us to hypothesize a gene-environment interaction for SZ in the form of immune challenge. We used month of birth as a proxy for environmental immune challenge and estimated the genetic correlation between winter-born and non-winter born SZ to be significantly less than 1 for coding/regulatory region SNPs (0.56, s.e. 0.14, P = 0.00090). Our results are consistent with epidemiological observations of a negative relationship between SZ and RA reflecting, at least in part, genetic factors. Results of the month of birth analysis are consistent with pleiotropic effects of genetic variants dependent on environmental context. © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
    International Journal of Epidemiology 08/2015; DOI:10.1093/ije/dyv136 · 9.18 Impact Factor
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    ABSTRACT: A schizophrenia phenotype for paternal and maternal age effects on illness risk could benefit etiological research. As odor sensitivity is associated with variability in symptoms and cognition in schizophrenia, we examined if it was related to parental ages in patients and healthy controls. We tested Leukocyte Telomere Length (LTL) as an explanatory factor, as LTL is associated with paternal age and schizophrenia risk. Seventy-five DSM-IV patients and 46 controls were assessed for detection of PEA, WAIS-III for cognition, and LTL, assessed by qPCR. In healthy controls, but not schizophrenia patients, decreasing sensitivity was monotonically related to advancing parental ages, particularly in sons. The relationships between parental aging and odor sensitivity differed significantly for patients and controls (Fisher's R to Z: χ(2) = 6.95, P = 0.009). The groups also differed in the association of odor sensitivity with cognition; lesser sensitivity robustly predicted cognitive impairments in patients (<0.001), but these were unassociated in controls. LTL was unrelated to odor sensitivity and did not explain the association of lesser sensitivity with cognitive deficits.Parental aging predicted less sensitive detection in healthy subjects but not in schizophrenia patients. In patients, decreased odor sensitivity strongly predicted cognitive deficits, whereas more sensitive acuity was associated with older parents. These data support separate risk pathways for schizophrenia. A parental age-related pathway may produce psychosis without impairing cognition and odor sensitivity. Diminished odor sensitivity may furthermore be useful as a biomarker for research and treatment studies in schizophrenia. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 07/2015; DOI:10.1002/ajmg.b.32351 · 3.42 Impact Factor
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    ABSTRACT: Advanced paternal age (APA) is a risk factor for schizophrenia (Sz) and bipolar disorder (BP). Putative mechanisms include heritable genetic factors, de novo mutations, and epigenetic mechanisms. Few studies have explored phenotypic features associated with APA. The Genomic Psychiatry Cohort established a clinically characterized repository of genomic samples from subjects with a Sz-BP diagnosis or unaffected controls, 12,975 with parental age information. We estimated relative risk ratios for Sz, schizoaffective depressed and bipolar types (SA-D, SA-B), and BP with and without history of psychotic features (PF) relative to the control group, comparing each paternal age group to the reference group 20–24 years. All tests were two-sided with adjustment for multiple comparisons. Subjects with fathers age 45+ had significantly higher risk for all diagnoses except for BP w/o PF. APA also bore no significant relation to family psychiatric history. In conclusion, we replicated APA as a risk factor for Sz. To our knowledge, this is the first published report of APA in a BP sample stratified by psychosis history, extending this association only in BP w/PF. This suggests that phenotypic expression of the APA effect in Sz-BP spectrum is psychosis, per se, rather than other aspects of these complex disorders. The lack of a significant relationship between paternal age and familial disease patterns suggests that underlying mechanisms of the paternal age effect may involve a complex interaction of heritable and non-heritable factors. The authors discuss implications and testable hypotheses, starting with a focus on genetic mechanisms and endophenotypic expressions of dopaminergic function.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 07/2015; DOI:10.1002/ajmg.b.32334 · 3.42 Impact Factor
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    ABSTRACT: Hundreds of genes reside in structurally complex, poorly understood regions of the human genome. One such region contains the three amylase genes (AMY2B, AMY2A and AMY1) responsible for digesting starch into sugar. Copy number of AMY1 is reported to be the largest genomic influence on obesity, although genome-wide association studies for obesity have found this locus unremarkable. Using whole-genome sequence analysis, droplet digital PCR and genome mapping, we identified eight common structural haplotypes of the amylase locus that suggest its mutational history. We found that the AMY1 copy number in an individual's genome is generally even (rather than odd) and partially correlates with nearby SNPs, which do not associate with body mass index (BMI). We measured amylase gene copy number in 1,000 obese or lean Estonians and in 2 other cohorts totaling ∼3,500 individuals. We had 99% power to detect the lower bound of the reported effects on BMI, yet found no association.
    Nature Genetics 06/2015; 47(8). DOI:10.1038/ng.3340 · 29.35 Impact Factor
  • 04/2015; 13(2):142-147. DOI:10.1176/appi.focus.130208
  • European Psychiatry; 03/2015
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    ABSTRACT: Genetic risk prediction has several potential applications in medical research and clinical practice and could be used, for example, to stratify a heterogeneous population of patients by their predicted genetic risk. However, for polygenic traits, such as psychiatric disorders, the accuracy of risk prediction is low. Here we use a multivariate linear mixed model and apply multi-trait genomic best linear unbiased prediction for genetic risk prediction. This method exploits correlations between disorders and simultaneously evaluates individual risk for each disorder. We show that the multivariate approach significantly increases the prediction accuracy for schizophrenia, bipolar disorder, and major depressive disorder in the discovery as well as in independent validation datasets. By grouping SNPs based on genome annotation and fitting multiple random effects, we show that the prediction accuracy could be further improved. The gain in prediction accuracy of the multivariate approach is equivalent to an increase in sample size of 34% for schizophrenia, 68% for bipolar disorder, and 76% for major depressive disorders using single trait models. Because our approach can be readily applied to any number of GWAS datasets of correlated traits, it is a flexible and powerful tool to maximize prediction accuracy. With current sample size, risk predictors are not useful in a clinical setting but already are a valuable research tool, for example in experimental designs comparing cases with high and low polygenic risk. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.
    The American Journal of Human Genetics 01/2015; 90. DOI:10.1016/j.ajhg.2014.12.006 · 10.93 Impact Factor
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    ABSTRACT: To examine the psychometric properties of the Brazilian Portuguese version of the Family Accommodation Scale for Obsessive-Compulsive Disorder – Interviewer-Rated (FAS-IR).MethodA total of 114 family members of patients with obsessive-compulsive disorder (OCD) were assessed. The following analyses of the FAS-IR were carried out: internal consistency, inter-rater and test-retest reliability, and exploratory factor analysis.ResultsThe Brazilian Portuguese version of the FAS-IR showed excellent inter-rater reliability (intraclass correlation coefficient [ICC] = 0.94) and acceptable test-retest reliability (ICC = 0.77), with no significant differences in FAS-IR scores. Factor analysis produced three factors for the scale. However, factor loadings were not well defined within each factor, and the factors did not have distinct constructs. Thus, a global analysis approach was chosen, revealing good internal consistency of the scale as a whole (Cronbach’s α = 0.805).Conclusions The Brazilian Portuguese FAS-IR showed sound psychometric properties for the evaluation of family accommodation, and is, therefore, a reliable instrument for use in research and clinical practice.
    Comprehensive Psychiatry 11/2014; 57. DOI:10.1016/j.comppsych.2014.11.017 · 2.25 Impact Factor
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    ABSTRACT: Schizophrenia (SZ) genome-wide association studies (GWASs) have identified common risk variants in >100 susceptibility loci; however, the contribution of rare variants at these loci remains largely unexplored. One of the strongly associated loci spans MIR137 (miR137) and MIR2682 (miR2682), two microRNA genes important for neuronal function. We sequenced ∼6.9 kb MIR137/MIR2682 and upstream regulatory sequences in 2,610 SZ cases and 2,611 controls of European ancestry. We identified 133 rare variants with minor allele frequency (MAF) <0.5%. The rare variant burden in promoters and enhancers, but not insulators, was associated with SZ (p = 0.021 for MAF < 0.5%, p = 0.003 for MAF < 0.1%). A rare enhancer SNP, 1:g.98515539A>T, presented exclusively in 11 SZ cases (nominal p = 4.8 × 10(-4)). We further identified its risk allele T in 2 of 2,434 additional SZ cases, 11 of 4,339 bipolar (BP) cases, and 3 of 3,572 SZ/BP study controls and 1,688 population controls; yielding combined p values of 0.0007, 0.0013, and 0.0001 for SZ, BP, and SZ/BP, respectively. The risk allele T of 1:g.98515539A>T reduced enhancer activity of its flanking sequence by >50% in human neuroblastoma cells, predicting lower expression of MIR137/MIR2682. Both empirical and computational analyses showed weaker transcription factor (YY1) binding by the risk allele. Chromatin conformation capture (3C) assay further indicated that 1:g.98515539A>T influenced MIR137/MIR2682, but not the nearby DPYD or LOC729987. Our results suggest that rare noncoding risk variants are associated with SZ and BP at MIR137/MIR2682 locus, with risk alleles decreasing MIR137/MIR2682 expression. Copyright © 2014 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.
    The American Journal of Human Genetics 11/2014; 95(6). DOI:10.1016/j.ajhg.2014.11.001 · 10.93 Impact Factor
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    ABSTRACT: Objective: The authors sought to demonstrate that schizophrenia is a heterogeneous group of heritable disorders caused by different genotypic networks that cause distinct clinical syndromes. Method: In a large genome-wide association study of cases with schizophrenia and controls, the authors first identified sets of interacting single-nucleotide polymorphisms (SNPs) that cluster within particular individuals (SNP sets) regardless of clinical status. Second, they examined the risk of schizophrenia for each SNP set and tested replicability in two independent samples. Third, they identified genotypic networks composed of SNP sets sharing SNPs or subjects. Fourth, they identified sets of distinct clinical features that cluster in particular cases (phenotypic sets or clinical syndromes) without regard for their genetic background. Fifth, they tested whether SNP sets were associated with distinct phenotypic sets in a replicable manner across the three studies. Results: The authors identified 42 SNP sets associated with a 70% or greater risk of schizophrenia, and confirmed 34 (81%) or more with similar high risk of schizophrenia in two independent samples. Seventeen networks of SNP sets did not share any SNP or subject. These disjoint genotypic networks were associated with distinct gene products and clinical syndromes (i.e., the schizophrenias) varying in symptoms and severity. Associations between genotypic networks and clinical syndromes were complex, showing multifinality and equifinality. The interactive networks explained the risk of schizophrenia more than the average effects of all SNPs (24%). Conclusions: Schizophrenia is a group of heritable disorders caused by a moderate number of separate genotypic networks associated with several distinct clinical syndromes.
    American Journal of Psychiatry 09/2014; DOI:10.1176/appi.ajp.2014.14040435 · 12.30 Impact Factor
  • Sarah M Hartz · Laura J Bierut · Michele T Pato
    JAMA Psychiatry 08/2014; 71(8):969. DOI:10.1001/jamapsychiatry.2014.707 · 12.01 Impact Factor
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    ABSTRACT: Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia.
    Nature 07/2014; 511(7510):421-427. DOI:10.1038/nature13595 · 41.46 Impact Factor
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    ABSTRACT: OBJECTIVE Obsessive-compulsive disorder (OCD) and Tourette syndrome (TS) are heritable neurodevelopmental disorders with a partially shared genetic etiology. This study represents the first genome-wide investigation of large (>500 kb), rare (<1%) copy number variants (CNVs) in OCD and the largest genome-wide CNV analysis in TS to date. METHOD The primary analyses used a cross-disorder design for 2,699 case patients (1,613 ascertained for OCD, 1,086 ascertained for TS) and 1,789 controls. Parental data facilitated a de novo analysis in 348 OCD trios. RESULTS Although no global CNV burden was detected in the cross-disorder analysis or in secondary, disease-specific analyses, there was a 3.3-fold increased burden of large deletions previously associated with other neurodevelopmental disorders (p = .09). Half of these neurodevelopmental deletions were located in a single locus, 16p13.11 (5 case patient deletions: 0 control deletions, p = .08 in the current study, p = .025 compared to published controls). Three 16p13.11 deletions were confirmed de novo, providing further support for the etiological significance of this region. The overall OCD de novo rate was 1.4%, which is intermediate between published rates in controls (0.7%) and in individuals with autism or schizophrenia (2-4%). CONCLUSION Several converging lines of evidence implicate 16p13.11 deletions in OCD, with weaker evidence for a role in TS. The trend toward increased overall neurodevelopmental CNV burden in TS and OCD suggests that deletions previously associated with other neurodevelopmental disorders may also contribute to these phenotypes.
    Journal of the American Academy of Child and Adolescent Psychiatry 06/2014; 53(8):910-919. DOI:10.1016/j.jaac.2014.04.022 · 7.26 Impact Factor
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    ABSTRACT: Importance Although early mortality in severe psychiatric illness is linked to smoking and alcohol, to our knowledge, no studies have comprehensively characterized substance use behavior in severe psychotic illness. In particular, recent assessments of substance use in individuals with mental illness are based on population surveys that do not include individuals with severe psychotic illness.Objective To compare substance use in individuals with severe psychotic illness with substance use in the general population.Design, Setting, and Participants We assessed comorbidity between substance use and severe psychotic disorders in the Genomic Psychiatry Cohort. The Genomic Psychiatry Cohort is a clinically assessed, multiethnic sample consisting of 9142 individuals with the diagnosis of schizophrenia, bipolar disorder with psychotic features, or schizoaffective disorder, and 10 195 population control individuals.Main Outcomes and Measures Smoking (smoked >100 cigarettes in a lifetime), heavy alcohol use (>4 drinks/day), heavy marijuana use (>21 times of marijuana use/year), and recreational drug use.Results Relative to the general population, individuals with severe psychotic disorders have increased risks for smoking (odds ratio, 4.6; 95% CI, 4.3-4.9), heavy alcohol use (odds ratio, 4.0; 95% CI, 3.6-4.4), heavy marijuana use (odds ratio, 3.5; 95% CI, 3.2-3.7), and recreational drug use (odds ratio, 4.6; 95% CI, 4.3-5.0). All races/ethnicities (African American, Asian, European American, and Hispanic) and both sexes have greatly elevated risks for smoking and alcohol, marijuana, and drug use. Of specific concern, recent public health efforts that have successfully decreased smoking among individuals younger than age 30 years appear to have been ineffective among individuals with severe psychotic illness (interaction effect between age and severe mental illness on smoking initiation, P = 4.5 × 105).Conclusions and Relevance In the largest assessment of substance use among individuals with severe psychotic illness to date, we found the odds of smoking and alcohol and other substance use to be dramatically higher than recent estimates of substance use in mild mental illness.
    03/2014; 71(3):248. DOI:10.1001/jamapsychiatry.2013.3726
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    ABSTRACT: Obsessive-compulsive disorder (OCD) impacts family functioning as family members modify their personal and family routines, participate in rituals, and provide reassurance. These behaviors have been identified as family accommodation (FA), a phenomenon that, if ignored, may facilitate OCD symptoms and lead to poorer prognosis. Because FA has been recognized as a predictor of treatment outcome, we examined the prevalence of FA and identified patient and family socio-demographic and clinical variables associated with FA in an outpatient sample. The study comprised 228 subjects, namely, 114 patients with OCD and 114 family members, assessed before the patients entered a 12-session cognitive-behavioral group therapy program. A multivariate linear regression model was used to control for confounding factors and to evaluate variables independently associated with FA. FA was evaluated using the Family Accommodation Scale for Obsessive-Compulsive Disorder - Interviewer Rated (FAS-IR). FA was found to be highly prevalent among family members. Two patient factors positively associated with FA were OCD severity as measured by the Clinical Global Impressions Scale (CGI) and higher scores on the Obsessions dimension of the Obsessive-Compulsive Inventory - Revised (OCI-R). Family members' characteristics positively associated with FA were higher scores on the OCI-R hoarding subscale and being the patient's spouse. Our findings suggest that the early identification of patients and family members who could benefit from interventions aimed at reducing FA could improve treatment outcomes.
    Psychiatry and Clinical Neurosciences 02/2014; 68(8). DOI:10.1111/pcn.12172 · 1.63 Impact Factor
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    ABSTRACT: Prior genome-scans of bipolar disorder have revealed chromosome 6q22 as a promising candidate region. However, linkage disequilibrium (LD) mapping studies have yet to identify replicated susceptibility loci. We analyzed 1,422 LD-tagging single nucleotide polymorphisms (SNPs) in 83 genes to test single-marker and locus-wide evidence of association with bipolar disorder in the NIMH Genetics Initiative bipolar pedigrees and the Portuguese Island Collection (PIC) (N = 1,093 in 528 informative pairs). Both studies previously demonstrated significant evidence of linkage to 6q. SNPs were genotyped using an Illumina iSelect genotyping array which employs the Infinium assay. Evidence of single-marker association was assessed using the generalized disequilibrium test (GDT). Empirical estimates of gene-wide significance were obtained by permutation (via 100,000 gene-dropping simulations) of Fisher's combined test of P-values for each locus. No single variant yielded significant experiment-wide evidence of association, for either the combined sample or in each subsample. Our gene-dropping simulations identified nominally significant gene-wide associations with multiple loci, of which NT5DC1 in the NIMH subsample and CCNC in the PIC were the strongest candidates. However, no one gene consistently exceeded empirical significance criteria in both independent samples or survived Bonferroni correction for the number of genes tested. Using a gene-based approach to family-based association, we identified gene-wide associations with several genes, though no single locus was significantly associated with bipolar disorder in both cohorts. This suggests that chromosome 6q may harbor multiple susceptibility loci or that complex patterns of LD in this region may confound approaches based on common SNPs. © 2013 Wiley Periodicals, Inc. This article is a U.S. Government work and is in the public domain in the USA.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 12/2013; 162(8). DOI:10.1002/ajmg.b.32200 · 3.42 Impact Factor
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    ABSTRACT: A number of large, rare copy number variants (CNVs) are deleterious for neurodevelopmental disorders, but large, rare, protective CNVs have not been reported for such phenotypes. Here we show in a CNV analysis of 47 005 individuals, the largest CNV analysis of schizophrenia to date, that large duplications (1.5–3.0 Mb) at 22q11.2—the reciprocal of the well-known, risk-inducing deletion of this locus—are substantially less common in schizophrenia cases than in the general population (0.014% vs 0.085%, OR=0.17, P=0.00086). 22q11.2 duplications represent the first putative protective mutation for schizophrenia.
    Molecular Psychiatry 11/2013; 19(1):37-40. DOI:10.1038/mp.2013.156 · 14.50 Impact Factor

Publication Stats

5k Citations
522.99 Total Impact Points


  • 2009–2015
    • University of Southern California
      • • Department of Psychiatry and Behavioral Sciences
      • • Keck School of Medicine
      Los Ángeles, California, United States
  • 2014
    • Keck School of Medicine USC
      Los Ángeles, California, United States
  • 2013–2014
    • University of California, Los Angeles
      Los Ángeles, California, United States
  • 2007
    • University at Albany, The State University of New York
      New York City, New York, United States
  • 2003–2007
    • State University of New York Upstate Medical University
      Syracuse, New York, United States
  • 2000–2006
    • University at Buffalo, The State University of New York
      • Department of Psychiatry
      Buffalo, NY, United States
  • 2005
    • Minneapolis Veterans Affairs Hospital
      Minneapolis, Minnesota, United States
  • 2003–2004
    • University of Toronto
      • Department of Psychiatry
      Toronto, Ontario, Canada
  • 2001
    • University of Coimbra
      Coímbra, Coimbra, Portugal
    • Buffalo Psychiatric Center
      Buffalo, New York, United States
  • 1995
    • Rhode Island Hospital
      Providence, Rhode Island, United States
  • 1993
    • Brown University
      • Department of Psychiatry and Human Behavior
      Providence, RI, United States