oru.sePublications
Change search
Refine search result
1 - 6 of 6
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the 'Create feeds' function.
  • 1.
    O'Gorman, A.
    et al.
    Department of Psychiatry, Royal College of Surgeons in Ireland (RCSI), Beaumont Hospital, Dublin, Ireland; Institute of Food and Health, UCD School of Agriculture and Food Science, University College Dublin (UCD), Belfield, Dublin, Ireland.
    Suvitaival, T.
    Steno Diabetes Center, Gentofte, Denmark.
    Ahonen, L.
    Steno Diabetes Center, Gentofte, Denmark.
    Cannon, M.
    Department of Psychiatry, Royal College of Surgeons in Ireland (RCSI), Beaumont Hospital, Dublin, Ireland.
    Zammit, S.
    MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, UK; Centre for Academic Mental Health, School of Social & Community Medicine, University of Bristol, Bristol, UK.
    Lewis, G.
    Division of Psychiatry, University College London, London, UK.
    Roche, H. M.
    Nutrigenomics Research Group, UCD Conway Institute/UCD Institute of Food & Health, School of Public Health, Physiotherapy & Sports Science, Univer sity College Dublin (UCD), Belfield, Dublin, Ireland.
    Mattila, I.
    Steno Diabetes Center, Gentofte, Denmark.
    Hyötyläinen, Tuulia
    Örebro University, School of Science and Technology. Steno Diabetes Center, Gentofte, Denmark; Department of Chemistry, Örebro University, Örebro, Sweden.
    Oresic, Matej
    Örebro University, School of Medical Sciences. Steno Diabetes Center, Gentofte, Denmark; Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.
    Brennan, L.
    Institute of Food and Health, UCD School of Agriculture and Food Science, University College Dublin (UCD), Belfield, Dublin, Ireland.
    Cotter, D. R.
    Department of Psychiatry, Royal College of Surgeons in Ireland (RCSI), Beaumont Hospital, Dublin, Ireland.
    Identification of a plasma signature of psychotic disorder in children and adolescents from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort2017In: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 7, article id e1240Article in journal (Refereed)
    Abstract [en]

    The identification of an early biomarker of psychotic disorder is important as early treatment is associated with improved patient outcome. Metabolomic and lipidomic approaches in combination with multivariate statistical analysis were applied to identify plasma alterations in children (age 11) (38 cases vs 67 controls) and adolescents (age 18) (36 cases vs 117 controls) preceeding or coincident with the development of psychotic disorder (PD) at age 18 in the Avon Longitudinal Study of Parents and Children (ALSPAC). Overall, 179 lipids were identified at age 11, with 32 found to be significantly altered between the control and PD groups. Following correction for multiple comparisons, 8 of these lipids remained significant (lysophosphatidlycholines (LPCs) LPC(18: 1), LPC(18: 2), LPC(20: 3); phosphatidlycholines (PCs) PC(32: 2; PC(34: 2), PC(36: 4), PC(0-34-3) and sphingomyelin (SM) SM(d18: 1/24: 0)), all of which were elevated in the PD group. At age 18, 23 lipids were significantly different between the control and PD groups, although none remained significant following correction for multiple comparisons. In conclusion, the findings indicate that the lipidome is altered in the blood during childhood, long before the development of psychotic disorder. LPCs in particular are elevated in those who develop PD, indicating inflammatory abnormalities and altered phospholipid metabolism. These findings were not found at age 18, suggesting there may be ongoing alterations in the pathophysiological processes from prodrome to onset of PD.

  • 2.
    Orešič, Matej
    et al.
    VTT Technical Research Centre of Finland, Tietotie 2, Espoo, FI-02044 VTT, Finland.
    Hyötyläinen, Tuulia
    Örebro University, School of Science and Technology. VTT Technical Research Centre of Finland, Tietotie 2, Espoo, FI-02044 VTT, Finland.
    Herukka, S-K
    Department of Neurology, Kuopio University Hospital, University of Eastern Finland, Kuopio, Finland.
    Sysi-Aho, M
    VTT Technical Research Centre of Finland, Tietotie 2, Espoo, FI-02044 VTT, Finland.
    Mattila, I
    VTT Technical Research Centre of Finland, Tietotie 2, Espoo, FI-02044 VTT, Finland.
    Seppänan-Laakso, T
    VTT Technical Research Centre of Finland, Tietotie 2, Espoo, FI-02044 VTT, Finland.
    Julkunen, V
    Department of Neurology, Kuopio University Hospital, University of Eastern Finland, Kuopio, Finland.
    Gopalacharyulu, P V
    VTT Technical Research Centre of Finland, Tietotie 2, Espoo, FI-02044 VTT, Finland.
    Hallikainen, M
    Department of Neurology, Kuopio University Hospital, University of Eastern Finland, Kuopio, Finland.
    Koikkalainen, J
    VTT Technical Research Centre of Finland, Tampere, Finland.
    Kivipelto, M
    Aging Research Center, Karolinska Institute, Stockholm, Sweden.
    Helisalmi, S
    Department of Neurology, Kuopio University Hospital, University of Eastern Finland, Kuopio, Finland.
    Lötjönen, J
    VTT Technical Research Centre of Finland, Tampere, Finland.
    Soininen, H
    Metabolome in progression to Alzheimer's disease2011In: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 1, article id e57Article in journal (Refereed)
    Abstract [en]

    Mild cognitive impairment (MCI) is considered as a transition phase between normal aging and Alzheimer's disease (AD). MCI confers an increased risk of developing AD, although the state is heterogeneous with several possible outcomes, including even improvement back to normal cognition. We sought to determine the serum metabolomic profiles associated with progression to and diagnosis of AD in a prospective study. At the baseline assessment, the subjects enrolled in the study were classified into three diagnostic groups: healthy controls (n=46), MCI (n=143) and AD (n=47). Among the MCI subjects, 52 progressed to AD in the follow-up. Comprehensive metabolomics approach was applied to analyze baseline serum samples and to associate the metabolite profiles with the diagnosis at baseline and in the follow-up. At baseline, AD patients were characterized by diminished ether phospholipids, phosphatidylcholines, sphingomyelins and sterols. A molecular signature comprising three metabolites was identified, which was predictive of progression to AD in the follow-up. The major contributor to the predictive model was 2,4-dihydroxybutanoic acid, which was upregulated in AD progressors (P=0.0048), indicating potential involvement of hypoxia in the early AD pathogenesis. This was supported by the pathway analysis of metabolomics data, which identified upregulation of pentose phosphate pathway in patients who later progressed to AD. Together, our findings primarily implicate hypoxia, oxidative stress, as well as membrane lipid remodeling in progression to AD. Establishment of pathogenic relevance of predictive biomarkers such as ours may not only facilitate early diagnosis, but may also help identify new therapeutic avenues.

  • 3.
    Polderman, T. J. C.
    et al.
    Department of Functional Genomics, Complex Trait Genetics, Center for Neurogenomics and Cognitive Research (CNCR), VU University Amsterdam, Amsterdam, The Netherlands.
    Hoekstra, R. A.
    Department of Life, Health and Chemical Sciences, Faculty of Science, The Open University, Milton Keynes, UK.
    Posthuma, D.
    Department of Functional Genomics, Complex Trait Genetics, Center for Neurogenomics and Cognitive Research (CNCR), VU University Amsterdam, Amsterdam, The Netherlands.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    The co-occurrence of autistic and ADHD dimensions in adults: an etiological study in 17,770 twins2014In: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 4, article id e435Article in journal (Refereed)
    Abstract [en]

    Autism spectrum disorder (ASD) and attention deficit/hyperactivity disorder (ADHD) often occur together. To obtain more insight in potential causes for the co-occurrence, this study examined the genetic and environmental etiology of the association between specific ASD and ADHD disorder dimensions. Self-reported data on ASD dimensions social and communication difficulties (ASDsc), and repetitive and restricted behavior and interests (ASDr), and ADHD dimensions inattention (IA), and hyperactivity/impulsivity (HI) were assessed in a community sample of 17,770 adult Swedish twins. Phenotypic, genetic and environmental associations between disorder dimensions were examined in a multivariate model, accounting for sex differences. ASDr showed the strongest associations with IA and HI in both sexes (r(p) 0.33 to 0.40). ASDsc also correlated moderately with IA (females r(p) 0.29 and males r(p) 0.35) but only modestly with HI (females r(p) 0.17 and males r(p) 0.20). Genetic correlations ranged from 0.22 to 0.64 and were strongest between ASDr and IA and HI. Sex differences were virtually absent. The ASDr dimension (reflecting restricted, repetitive and stereotyped patterns of behavior, interests and activities) showed the strongest association with dimensions of ADHD, on a phenotypic, genetic and environmental level. This study opens new avenues for molecular genetic research. As our findings demonstrated that genetic overlap between disorders is dimension-specific, future gene-finding studies on psychiatric comorbidity should focus on carefully selected genetically related dimensions of disorders.

  • 4.
    Sariaslan, A.
    et al.
    Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, UK; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fazel, S.
    Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, UK.
    D'Onofrio, B. M.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Långström, N.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bergen, S. E.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Kuja-Halkola, R.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Schizophrenia and subsequent neighborhood deprivation: revisiting the social drift hypothesis using population, twin and molecular genetic data2016In: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 6, article id e796Article in journal (Refereed)
    Abstract [en]

    Neighborhood influences in the etiology of schizophrenia have been emphasized in a number of systematic reviews, but causality remains uncertain. To test the social drift hypothesis, we used three complementary genetically informed Swedish cohorts. First, we used nationwide Swedish data on approximately 760 000 full- and half-sibling pairs born between 1951 and 1974 and quantitative genetic models to study genetic and environmental influences on the overlap between schizophrenia in young adulthood and subsequent residence in socioeconomically deprived neighborhoods. Schizophrenia diagnoses were ascertained using the National Patient Registry. Second, we tested the overlap between childhood psychotic experiences and neighborhood deprivation in early adulthood in the longitudinal Twin Study of Child and Adolescent Development (TCHAD; n=2960). Third, we investigated to what extent polygenic risk scores for schizophrenia predicted residence in deprived neighborhoods during late adulthood using the TwinGene sample (n=6796). Sibling data suggested that living in deprived neighborhoods was substantially heritable; 65% (95% confidence interval (95% CI): 60-71%) of the variance was attributed to genetic influences. Although the correlation between schizophrenia and neighborhood deprivation was moderate in magnitude (r=0.22; 95% CI: 0.20-0.24), it was entirely explained by genetic influences. We replicated these findings in the TCHAD sample. Moreover, the association between polygenic risk for schizophrenia and neighborhood deprivation was statistically significant (R(2)=0.15%, P=0.002). Our findings are primarily consistent with a genetic selection interpretation where genetic liability for schizophrenia also predicts subsequent residence in socioeconomically deprived neighborhoods. Previous studies may have overemphasized the relative importance of environmental influences in the social drift of schizophrenia patients. Clinical and policy interventions will therefore benefit from the future identification of potentially causal pathways between different dimensions of cognitive functions and socioeconomic trajectories derived from studies adopting family-based research designs.

  • 5.
    Suvitaival, T.
    et al.
    Steno Diabetes Center, Gentofte, Denmark.
    Mantere, O.
    Mental Health Unit, National Institute for Health and Welfare, Helsinki, Finland; Department of Psychiatry, McGill University, Montréal, QC, Canada; Bipolar Disorders Clinic, Douglas Mental Health University Institute, Montréal, QC, Canada.
    Kieseppä, T.
    Mental Health Unit, National Institute for Health and Welfare, Helsinki, Finland; Department of Psychiatry, Helsinki University and Helsinki University Hospital, Helsinki, Finland.
    Mattila, I.
    Steno Diabetes Center, Gentofte, Denmark.
    Pöhö, P.
    Faculty of Pharmacy, University of Helsinki, Helsinki, Finland.
    Hyötyläinen, Tuulia
    Örebro University, School of Science and Technology. Steno Diabetes Center, Gentofte, Denmark.
    Suvisaari, J.
    Mental Health Unit, National Institute for Health and Welfare, Helsinki, Finland.
    Orešič, M.
    Steno Diabetes Center, Gentofte, Denmark; Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.
    Serum metabolite profile associates with the development of metabolic co-morbidities in first-episode psychosis2016In: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 6, no 11, article id e951Article in journal (Refereed)
    Abstract [en]

    Psychotic patients are at high risk for developing obesity, metabolic syndrome and type 2 diabetes. These metabolic co-morbidities are hypothesized to be related to both treatment side effects as well as to metabolic changes occurring during the psychosis. Earlier metabolomics studies have shown that blood metabolite levels are predictive of insulin resistance and type 2 diabetes in the general population as well as sensitive to the effects of antipsychotics. In this study, we aimed to identify the metabolite profiles predicting future weight gain and other metabolic abnormalities in psychotic patients. We applied comprehensive metabolomics to investigate serum metabolite profiles in a prospective study setting in 36 first-episode psychosis patients during the first year of the antipsychotic treatment and 19 controls. While corroborating several earlier findings when comparing cases and controls and the effects of the antipsychotic medication, we also found that prospective weight gain in psychotic patients was associated with increased levels of triacylglycerols with low carbon number and double-bond count at baseline, that is, lipids known to be associated with increased liver fat. Our study suggests that metabolite profiles may be used to identify the psychotic patients most vulnerable to develop metabolic co-morbidities, and may point to a pharmacological approach to counteract the antipsychotic-induced weight gain.

  • 6.
    Zayats, T
    et al.
    K.G. Jebsen Centre for Neuropsychiatric Disorders, Department of Biomedicine, University of Bergen, Bergen, Norway.
    Jacobsen, K K
    K.G. Jebsen Centre for Neuropsychiatric Disorders, Department of Biomedicine, University of Bergen, Bergen, Norway.
    Kleppe, R
    K.G. Jebsen Centre for Neuropsychiatric Disorders, Department of Biomedicine, University of Bergen, Bergen, Norway.
    Jacob, C P
    Section of Molecular Psychiatry, Clinical Research Unit on Disorders of Neurodevelopment and Cognition Center of Mental Health, University of Wuerburg, Würzburg, Germany.
    Kittel-Schneider, S
    Department of Psychiatry, Psychosomatic Medicine and Psychotherapy, University Hospital Frankfurt, Frankfurt am Main, Germany.
    Ribasés, M
    Psychiatric Genetics Unit, Group of Psychiatry, Mental Health and Addictions, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Department of Psychiatry, Hospital Universitari Vall d'Hebron, Barcelona, Spain; Biomedical Network Research Centre on Mental Health (CIBERSAM), Madrid, Spain.
    Ramos-Quiroga, J A
    Psychiatric Genetics Unit, Group of Psychiatry, Mental Health and Addictions, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Department of Psychiatry, Hospital Universitari Vall d'Hebron, Barcelona, Spain; Biomedical Network Research Centre on Mental Health (CIBERSAM), Madrid, Spain; Departments of Psychiatry and Legal Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain.
    Richarte, V
    Psychiatric Genetics Unit, Group of Psychiatry, Mental Health and Addictions, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Department of Psychiatry, Hospital Universitari Vall d'Hebron, Barcelona, Spain; Biomedical Network Research Centre on Mental Health (CIBERSAM), Madrid, Spain; Departments of Psychiatry and Legal Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain.
    Casas, M
    Psychiatric Genetics Unit, Group of Psychiatry, Mental Health and Addictions, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Department of Psychiatry, Hospital Universitari Vall d'Hebron, Barcelona, Spain; Biomedical Network Research Centre on Mental Health (CIBERSAM), Madrid, Spain; Departments of Psychiatry and Legal Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain.
    Mota, N R
    Department of Genetics, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
    Grevet, E H
    Department of Psychiatry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
    Klein, M
    Department of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
    Corominas, J
    Department of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands; Department of Ophtalmology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands.
    Bralten, J
    Department of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
    Galesloot, T
    Department for Health Evidence, Radboud Institute for Health Sciences, Radboud University Medical Center, Nijmegen, The Netherlands.
    Vasquez, A A
    Department of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands; Department of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands; Department of Psychiatry, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
    Herms, S
    Institute of Human Genetics, University of Bonn, Bonn, Germany; Department of Genomics, Life and Brain Center, Bonn, Germany; Department of Biomedicine, University of Basel, Basel, Switzerland.
    Forstner, A J
    Institute of Human Genetics, University of Bonn, Bonn, Germany; Department of Genomics, Life and Brain Center, Bonn, Germany.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Breen, G
    NIHR BRC for Mental Health, Institute of Psychiatry, Psychology and Neuroscience and SLaM NHS Trust, King's College London, London, UK; MRC Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
    Asherson, P
    NIHR BRC for Mental Health, Institute of Psychiatry, Psychology and Neuroscience and SLaM NHS Trust, King's College London, London, UK; MRC Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
    Gross-Lesch, S
    Section of Molecular Psychiatry, Clinical Research Unit on Disorders of Neurodevelopment and Cognition Center of Mental Health, University of Wuerburg, Würzburg, Germany.
    Lesch, K P
    Section of Molecular Psychiatry, Clinical Research Unit on Disorders of Neurodevelopment and Cognition Center of Mental Health, University of Wuerburg, Würzburg, Germany.
    Cichon, S
    Department of Genomics, Life and Brain Center, Bonn, Germany; Department of Biomedicine, University of Basel, Basel, Switzerland; Institute of Neuroscience and Medicine, Structural and Functional Organization of the Brain (INM-1), Research Center Juelich, Juelich, Germany.
    Gabrielsen, M B
    K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health, NTNU, Norwegian University of Science and Technology, Trondheim, Norway; Department of Laboratory Medicine, Children's and Women's Health, Norwegian University of Science and Technology, Trondheim, Norway.
    Holmen, O L
    K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
    Bau, C H D
    Department of Genetics, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
    Buitelaar, J
    Department of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
    Kiemeney, L
    Department for Health Evidence, Radboud Institute for Health Sciences, Radboud University Medical Center, Nijmegen, The Netherlands.
    Faraone, S V
    K.G. Jebsen Centre for Neuropsychiatric Disorders, Department of Biomedicine, University of Bergen, Bergen, Norway; Departments of Psychiatry and of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, NY, USA.
    Cormand, B
    Departament de Genètica, Microbiologia i Estadística, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain; Centro de Investigación BiomédicaAnchor en Red de Enfermedades Raras, Barcelona, Spain; Institut de Biomedicina de la Universitat de Barcelona, Barcelona, Spain; Institut de Recerca Pediàtrica HosAnchorpital Sant Joan de Déu, Barcelona, Spain.
    Franke, B
    Department of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands; Department of Psychiatry, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
    Reif, A
    Department of Psychiatry, Psychosomatic Medicine and Psychotherapy, University Hospital Frankfurt, Frankfurt am Main, Germany.
    Haavik, J
    K.G. Jebsen Centre for Neuropsychiatric Disorders, Department of Biomedicine, University of Bergen, Bergen, Norway; Division of Psychiatry, Haukeland University Hospital, Bergen, Norway.
    Johansson, S
    K.G. Jebsen Centre for Neuropsychiatric Disorders, Department of Clinical Science, University of Bergen, Bergen, Norway; Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway.
    Exome chip analyses in adult attention deficit hyperactivity disorder2016In: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 6, no 10, article id e923Article in journal (Refereed)
    Abstract [en]

    Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable childhood-onset neuropsychiatric condition, often persisting into adulthood. The genetic architecture of ADHD, particularly in adults, is largely unknown. We performed an exome-wide scan of adult ADHD using the Illumina Human Exome Bead Chip, which interrogates over 250 000 common and rare variants. Participants were recruited by the International Multicenter persistent ADHD CollaboraTion (IMpACT). Statistical analyses were divided into 3 steps: (1) gene-level analysis of rare variants (minor allele frequency (MAF)<1%); (2) single marker association tests of common variants (MAF⩾1%), with replication of the top signals; and (3) pathway analyses. In total, 9365 individuals (1846 cases and 7519 controls) were examined. Replication of the most associated common variants was attempted in 9847 individuals (2077 cases and 7770 controls) using fixed-effects inverse variance meta-analysis. With a Bonferroni-corrected significance level of 1.82E-06, our analyses of rare coding variants revealed four study-wide significant loci: 6q22.1 locus (P=4.46E-08), where NT5DC1 and COL10A1 reside; the SEC23IP locus (P=6.47E-07); the PSD locus (P=7.58E-08) and ZCCHC4 locus (P=1.79E-06). No genome-wide significant association was observed among the common variants. The strongest signal was noted at rs9325032 in PPP2R2B (odds ratio=0.81, P=1.61E-05). Taken together, our data add to the growing evidence of general signal transduction molecules (NT5DC1, PSD, SEC23IP and ZCCHC4) having an important role in the etiology of ADHD. Although the biological implications of these findings need to be further explored, they highlight the possible role of cellular communication as a potential core component in the development of both adult and childhood forms of ADHD.

1 - 6 of 6
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf