Michele T Pato

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

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Publications (106)534.04 Total impact

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    ABSTRACT: Genome-wide association studies (GWAS) of schizophrenia have yielded more than 100 common susceptibility variants, and strongly support a substantial polygenic contribution of a large number of small allelic effects. It has been hypothesized that familial schizophrenia is largely a consequence of inherited rather than environmental factors. We investigated the extent to which familiality of schizophrenia is associated with enrichment for common risk variants detectable in a large GWAS. We analyzed single nucleotide polymorphism (SNP) data for cases reporting a family history of psychotic illness (N=978), cases reporting no such family history (N=4,503), and unscreened controls (N=8,285) from the Psychiatric Genomics Consortium (PGC1) study of schizophrenia. We used a multinomial logistic regression approach with model-fitting to detect allelic effects specific to either family history subgroup. We also considered a polygenic model, in which we tested whether family history positive subjects carried more schizophrenia risk alleles than family history negative subjects, on average. Several individual SNPs attained suggestive but not genome-wide significant association with either family history subgroup. Comparison of genome-wide polygenic risk scores based on GWAS summary statistics indicated a significant enrichment for SNP effects among family history positive compared to family history negative cases (Nagelkerke's R2=0.0021; P=0.00331; P-value threshold <0.4). Estimates of variability in disease liability attributable to the aggregate effect of genome-wide SNPs were significantly greater for family history positive compared to family history negative cases (0.32 and 0.22, respectively; P=0.031). We found suggestive evidence of allelic effects detectable in large GWAS of schizophrenia that might be specific to particular family history subgroups. However, consideration of a polygenic risk score indicated a significant enrichment among family history positive cases for common allelic effects. Familial illness might, therefore, represent a more heritable form of schizophrenia, as suggested by previous epidemiological studies.
    No preview · Article · Dec 2015 · American Journal of Medical Genetics Part B Neuropsychiatric Genetics
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    ABSTRACT: Several studies have reported differences between African Americans and Caucasians in relative proportion of psychotic symptoms and disorders, but whether this reflects racial bias in the assessment of psychosis is unclear. The purpose of this study was to examine the distribution of psychotic symptoms and potential bias in symptoms assessed via semi-structured interview using a cohort of 3,389 African American and 5,692 Caucasian participants who were diagnosed with schizophrenia, schizoaffective disorder, or bipolar disorder. In this cohort, the diagnosis of schizophrenia was relatively more common, and the diagnosis of bipolar disorder and schizoaffective disorder-bipolar type was less relatively common, among African Americans than Caucasians. With regard to symptoms, relatively more African Americans than Caucasians endorsed hallucinations and delusions symptoms, and this pattern was striking among cases diagnosed with bipolar disorder and schizoaffective-bipolar disorder. In contrast, the relative endorsement of psychotic symptoms was more similar among cases diagnosed with schizophrenia and schizoaffective disorder-depressed type. Differential item function analysis revealed that African Americans with mild psychosis over-endorsed "hallucinations in any modality" and under-endorsed "widespread delusions" relative to Caucasians. Other symptoms did not show evidence of racial bias. Thus, racial bias in assessment of psychotic symptoms does not appear to explain differences in the proportion of symptoms between Caucasians and African Americans. Rather, this may reflect ascertainment bias, perhaps indicative of a disparity in access to services, or differential exposure to risk factors for psychosis by race.
    No preview · Article · Dec 2015 · American Journal of Medical Genetics Part B Neuropsychiatric Genetics
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    ABSTRACT: Polygenic risk scores have shown great promise in predicting complex disease risk and will become more accurate as training sample sizes increase. The standard approach for calculating risk scores involves linkage disequilibrium (LD)-based marker pruning and applying a p value threshold to association statistics, but this discards information and can reduce predictive accuracy. We introduce LDpred, a method that infers the posterior mean effect size of each marker by using a prior on effect sizes and LD information from an external reference panel. Theory and simulations show that LDpred outperforms the approach of pruning followed by thresholding, particularly at large sample sizes. Accordingly, predicted R-2 increased from 20.1% to 25.3% in a large schizophrenia dataset and from 9.8% to 12.0% in a large multiple sclerosis dataset. A similar relative improvement in accuracy was observed for three additional large disease datasets and for non-European schizophrenia samples. The advantage of LDpred over existing methods will grow as sample sizes increase.
    Full-text · Article · Oct 2015 · The American Journal of Human Genetics
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    ABSTRACT: Patients with Bipolar disorder smoke more than the general population. Smoking negatively impacts mortality and clinical course in Bipolar disorder patients. Prior studies have shown contradictory results regarding the impact of psychosis on smoking behavior in Bipolar disorder. We analyzed a large sample of Bipolar disorder and Schizoaffective disorder, Bipolar Type patients and predicted those with a history of psychosis would be more likely to be nicotine dependent. Data from subjects and controls were collected from the Genomic Psychiatry Cohort (GPC). Subjects were diagnosed with Bipolar disorder without psychosis (N = 610), Bipolar disorder with psychosis (N = 1544). Participants were classified with or without nicotine dependence. Diagnostic groups were compared to controls (N = 10065) using logistic regression. Among smokers (N = 6157), those with Bipolar disorder had an increased risk of nicotine dependence (OR = 2.5; P < 0.0001). Patients with Bipolar disorder with psychosis were more likely to be dependent than Bipolar disorder patients without psychosis (OR = 1.3; P = 0.03). Schizoaffective disorder, Bipolar Type patients had more risk of nicotine dependence when compared to Bipolar disorder patients with or without psychosis (OR = 1.2; P = 0.02). Bipolar disorder patients experiencing more severity of psychosis have more risk of nicotine dependence. © 2015 Wiley Periodicals, Inc.
    No preview · Article · Oct 2015 · American Journal of Medical Genetics Part B Neuropsychiatric Genetics
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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.
    Full-text · Conference Paper · Sep 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.
    No preview · Article · Sep 2015 · American Journal of Medical Genetics Part B Neuropsychiatric Genetics
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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.
    Full-text · Article · Aug 2015 · International Journal of Epidemiology
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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.
    Full-text · Article · Jul 2015 · American Journal of Medical Genetics Part B Neuropsychiatric Genetics
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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.
    No preview · Article · Jul 2015 · American Journal of Medical Genetics Part B Neuropsychiatric Genetics
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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.
    Full-text · Article · Jun 2015 · Nature Genetics
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    ABSTRACT: Objectives To investigate the symptom dimensions of psychosis using factor analyses/FA of lifetime symptoms of a sample of Portuguese psychotic patients. Method FA of the OPCRIT items (56 signs and symptoms) of 684 patients - Schizophrenia/Sz (73.8%), Other non-organic psychotic disorders/ONPD (6.0), Schizoaffective disorders/SzA (1.4%), Bipolar disorders/BP (18.1%) and Severe depression with psychosis/SDP (.8%) – assessed with the Diagnostic Interview for Genetic Studies. Delusions of poverty, guilty delusions, nihilistic delusions, primary delusional perception, and somnolence, problems with appetite and weight and grandiosity were excluded from the final solution, as each were present in less than 10% of patients and did not load at any factor. Results Following the Kaiser and the Cattel's Scree Plot criteria, a four factors structure was selected, which explained variance (EV) was of 60.25%. Based on items content, the meaningful four factors were denominated as follows: F1 Depression (EV 21.77%; a=.97); F2 Mania (5.72%; a=.97); F3 Delusions and hallucinations (2.97%; a=.92); F4 Disorganization and Negative symptoms (2.07%; a=.90). Mann-Whitney U tests revealed that the symptom dimensions that distinguished better between Dx categories were Delusions and hallucinations (only SDP vs. BP and Sc vs. SzA did not significantly differ) and Disorganization and Negative symptoms (only SDP vs. BP and SDP vs. ONPD did not significantly differ), with Sz patients presenting the highest scores. Conclusions This factorial structure is in accordance with other reports. Given the Schizophrenia (Sz) and Bipolar disorder (BP) heterogeneity and overlap, the present study contribute to phenotypic refinement and formulation of alternative psychosis phenotypes.
    Full-text · Conference Paper · Jun 2015

  • No preview · Article · Apr 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.
    Full-text · Article · Jan 2015 · The American Journal of Human Genetics
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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.
    Full-text · Article · Nov 2014 · Comprehensive Psychiatry
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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.
    Full-text · Article · Nov 2014 · The American Journal of Human Genetics
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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.
    Full-text · Article · Sep 2014 · American Journal of Psychiatry
  • Sarah M Hartz · Laura J Bierut · Michele T Pato

    No preview · Article · Aug 2014 · JAMA Psychiatry
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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.
    Full-text · Article · Jul 2014 · Nature
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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.
    Full-text · Article · Jun 2014 · Journal of the American Academy of Child and Adolescent Psychiatry

  • No preview · Article · Apr 2014

Publication Stats

6k Citations
534.04 Total Impact Points

Institutions

  • 2013-2015
    • Keck School of Medicine USC
      Los Ángeles, California, United States
  • 2011-2015
    • University of California, Los Angeles
      • Department of Psychiatry and Biobehavioural Sciences
      Los Ángeles, California, United States
  • 2009-2015
    • University of Southern California
      • • Department of Psychiatry and Behavioral Sciences
      • • Keck School of Medicine
      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
  • 2006
    • Washington DC VA Medical Center
      Washington, Washington, D.C., 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
    • Georgetown University
      • Department of Psychiatry
      Washington, Washington, D.C., United States
  • 2003-2004
    • University of Toronto
      • Department of Psychiatry
      Toronto, Ontario, Canada
  • 2001
    • Erie County Medical Center
      Buffalo, New York, United States
    • 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