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  • 151.
    Zandian, A.
    et al.
    KTH Royal Inst Technol, Sch Biotechnol, Affin Prote, SciLifeLab, Tomtebodavagen 23A, S-17165 Stockholm, Sweden..
    Wingard, L.
    Karolinska Inst, Ctr Mol Med, Karolinska Univ Hosp Solna, Dept Clin Neurosci, L8 01, Stockholm, Sweden.;Karolinska Univ Hosp Solna, SLSO, Psykiatri Nordvast, Stockholm, Sweden.;Karolinska Inst, Karolinska Univ Hosp Solna, Ctr Pharmacoepidemiol, Dept Med, Stockholm, Sweden..
    Nilsson, H.
    Karolinska Inst, Ctr Mol Med, Karolinska Univ Hosp Solna, Dept Clin Neurosci, L8 01, Stockholm, Sweden..
    Sjöstedt, Evelina
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical and experimental pathology.
    Johansson, D. X.
    Karolinska Inst, Ctr Mol Med, Karolinska Univ Hosp Solna, Dept Clin Neurosci, L8 01, Stockholm, Sweden..
    Just, D.
    KTH Royal Inst Technol, Sch Biotechnol, Affin Prote, SciLifeLab, Tomtebodavagen 23A, S-17165 Stockholm, Sweden..
    Hellstrom, C.
    KTH Royal Inst Technol, Sch Biotechnol, Affin Prote, SciLifeLab, Tomtebodavagen 23A, S-17165 Stockholm, Sweden..
    Uhlen, M.
    KTH Royal Inst Technol, Sch Biotechnol, Affin Prote, SciLifeLab, Tomtebodavagen 23A, S-17165 Stockholm, Sweden..
    Schwenk, J. M.
    KTH Royal Inst Technol, Sch Biotechnol, Affin Prote, SciLifeLab, Tomtebodavagen 23A, S-17165 Stockholm, Sweden..
    Haemark-Manberg, A.
    KTH Royal Inst Technol, Sch Biotechnol, Affin Prote, SciLifeLab, Tomtebodavagen 23A, S-17165 Stockholm, Sweden..
    Norbeck, O.
    Karolinska Inst, Karolinska Univ Hosp Solna, Ctr Mol Med, Dept Med, L8 01, Stockholm, Sweden.;Karolinska Inst, Sect Psychiat, Karolinska Univ Hosp Huddinge, Dept Clin Neurosci,Ctr Psychiat Res, Stockholm, Sweden..
    Owe-Larsson, B.
    Karolinska Inst, Sect Psychiat, Karolinska Univ Hosp Huddinge, Dept Clin Neurosci,Ctr Psychiat Res, Stockholm, Sweden..
    Nilsson, P.
    KTH Royal Inst Technol, Sch Biotechnol, Affin Prote, SciLifeLab, Tomtebodavagen 23A, S-17165 Stockholm, Sweden..
    Persson, M. A. A.
    Karolinska Inst, Ctr Mol Med, Karolinska Univ Hosp Solna, Dept Clin Neurosci, L8 01, Stockholm, Sweden.;Karolinska Univ Hosp Solna, SLSO, Psykiatri Nordvast, Stockholm, Sweden..
    Untargeted screening for novel autoantibodies with prognostic value in first-episode psychosis2017In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 7, article id e1177Article in journal (Refereed)
    Abstract [en]

    Immunological and inflammatory reactions have been suggested to have a role in the development of schizophrenia, a hypothesis that has recently been supported by genetic data. The aim of our study was to perform an unbiased search for autoantibodies in patients with a first psychotic episode, and to explore the association between any seroreactivity and the development of a Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) disorder characterized by chronic or relapsing psychotic symptoms. We collected plasma samples from 53 patients when they were treated for their first-episode psychosis, and 41 non-psychotic controls, after which the patients were followed for a mean duration of 7 years. Thirty patients were diagnosed with schizophrenia, delusional disorder, schizoaffective disorder, bipolar disorder or a long-term unspecified nonorganic psychosis during follow-up, whereas 23 patients achieved complete remission. At the end of follow-up, plasma samples were analyzed for IgG reactivity to 2304 fragments of human proteins using a multiplexed affinity proteomic technique. Eight patient samples showed autoreactivity to the N-terminal fragment of the PAGE (P antigen) protein family (PAGE2B/PAGE2/PAGE5), whereas no such autoreactivity was seen among the controls. PAGE autoreactivity was associated with a significantly increased risk of being diagnosed with schizophrenia during follow-up (odds ratio 6.7, relative risk 4.6). An immunohistochemistry analysis using antisera raised against the N-terminal fragment stained an unknown extracellular target in human cortical brain tissue. Our findings suggest that autoreactivity to the N-terminal portion of the PAGE protein family is associated with schizophrenia in a subset of patients with first-episode psychosis.

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  • 152.
    Zandian, Arash
    et al.
    KTH, School of Biotechnology (BIO), Proteomics and Nanobiotechnology. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Wingård, L.
    Nilsson, H.
    Sjöstedt, E.
    Johansson, D. X.
    Just, David
    KTH, School of Biotechnology (BIO), Proteomics and Nanobiotechnology. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Hellström, Cecilia
    KTH, School of Biotechnology (BIO), Proteomics and Nanobiotechnology. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Uhlén, Mathias
    KTH, School of Biotechnology (BIO), Proteomics and Nanobiotechnology. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Schwenk, Jochen M.
    KTH, School of Biotechnology (BIO), Proteomics and Nanobiotechnology. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Häggmark-Månberg, Anna
    KTH, School of Biotechnology (BIO), Proteomics and Nanobiotechnology. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Norbeck, O.
    Owe-Larsson, B.
    Nilsson, Peter
    KTH, School of Biotechnology (BIO), Proteomics and Nanobiotechnology. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Persson, M. A. A.
    Untargeted screening for novel autoantibodies with prognostic value in first-episode psychosis2017In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 7, article id e1177Article in journal (Refereed)
    Abstract [en]

    Immunological and inflammatory reactions have been suggested to have a role in the development of schizophrenia, a hypothesis that has recently been supported by genetic data. The aim of our study was to perform an unbiased search for autoantibodies in patients with a first psychotic episode, and to explore the association between any seroreactivity and the development of a Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) disorder characterized by chronic or relapsing psychotic symptoms. We collected plasma samples from 53 patients when they were treated for their first-episode psychosis, and 41 non-psychotic controls, after which the patients were followed for a mean duration of 7 years. Thirty patients were diagnosed with schizophrenia, delusional disorder, schizoaffective disorder, bipolar disorder or a long-term unspecified nonorganic psychosis during follow-up, whereas 23 patients achieved complete remission. At the end of follow-up, plasma samples were analyzed for IgG reactivity to 2304 fragments of human proteins using a multiplexed affinity proteomic technique. Eight patient samples showed autoreactivity to the N-terminal fragment of the PAGE (P antigen) protein family (PAGE2B/PAGE2/PAGE5), whereas no such autoreactivity was seen among the controls. PAGE autoreactivity was associated with a significantly increased risk of being diagnosed with schizophrenia during follow-up (odds ratio 6.7, relative risk 4.6). An immunohistochemistry analysis using antisera raised against the N-terminal fragment stained an unknown extracellular target in human cortical brain tissue. Our findings suggest that autoreactivity to the N-terminal portion of the PAGE protein family is associated with schizophrenia in a subset of patients with first-episode psychosis.

  • 153.
    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 Wurzburg, 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 Wurzburg, Würzburg, Germany.
    Lesch, K P
    Section of Molecular Psychiatry, Clinical Research Unit on Disorders of Neurodevelopment and Cognition Center of Mental Health, University of Wurzburg, 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, 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.

  • 154. Ziermans, T
    et al.
    Dumontheil, I
    Roggeman, C
    Peyrard-Janvid, M
    Matsson, H
    Kere, J
    Klingberg, T
    Working memory brain activity and capacity link MAOA polymorphism to aggressive behavior during development.2012In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 2, article id e85Article in journal (Refereed)
    Abstract [en]

    A developmental increase in working memory capacity is an important part of cognitive development, and low working memory (WM) capacity is a risk factor for developing psychopathology. Brain activity represents a promising endophenotype for linking genes to behavior and for improving our understanding of the neurobiology of WM development. We investigated gene-brain-behavior relationships by focusing on 18 single-nucleotide polymorphisms (SNPs) located in six dopaminergic candidate genes (COMT, SLC6A3/DAT1, DBH, DRD4, DRD5, MAOA). Visuospatial WM (VSWM) brain activity, measured with functional magnetic resonance imaging, and VSWM capacity were assessed in a longitudinal study of typically developing children and adolescents. Behavioral problems were evaluated using the Child Behavior Checklist (CBCL). One SNP (rs6609257), located ~6.6 kb downstream of the monoamine oxidase A gene (MAOA) on human chromosome X, significantly affected brain activity in a network of frontal, parietal and occipital regions. Increased activity in this network, but not in caudate nucleus or anterior prefrontal regions, was correlated with VSWM capacity, which in turn predicted externalizing (aggressive/oppositional) symptoms, with higher WM capacity associated with fewer externalizing symptoms. There were no direct significant correlations between rs6609257 and behavioral symptoms. These results suggest a mediating role of WM brain activity and capacity in linking the MAOA gene to aggressive behavior during development.

  • 155.
    Zillich, Lea
    et al.
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Dept Genet Epidemiol Psychiat, Mannheim, Germany..
    Poisel, Eric
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Dept Genet Epidemiol Psychiat, Mannheim, Germany..
    Frank, Josef
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Dept Genet Epidemiol Psychiat, Mannheim, Germany..
    Foo, Jerome C.
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Dept Genet Epidemiol Psychiat, Mannheim, Germany..
    Friske, Marion M.
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Inst Psychopharmacol, Mannheim, Germany..
    Streit, Fabian
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Dept Genet Epidemiol Psychiat, Mannheim, Germany..
    Sirignano, Lea
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Dept Genet Epidemiol Psychiat, Mannheim, Germany..
    Heilmann-Heimbach, Stefanie
    Univ Bonn, Sch Med, Inst Human Genet, Bonn, Germany.;Univ Hosp Bonn, Bonn, Germany..
    Heimbach, Andre
    Univ Bonn, Sch Med, Inst Human Genet, Bonn, Germany.;Univ Hosp Bonn, Bonn, Germany..
    Hoffmann, Per
    Univ Bonn, Sch Med, Inst Human Genet, Bonn, Germany.;Univ Hosp Bonn, Bonn, Germany.;Univ Basel, Dept Biomed, CH-4003 Basel, Switzerland..
    Degenhardt, Franziska
    Univ Duisburg Essen, Univ Hosp Essen, Dept Child & Adolescent Psychiat, Essen, Germany..
    Hansson, Anita C.
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Inst Psychopharmacol, Mannheim, Germany..
    Bakalkin, Georgy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Nothen, Markus M.
    Univ Bonn, Sch Med, Inst Human Genet, Bonn, Germany.;Univ Hosp Bonn, Bonn, Germany..
    Rietschel, Marcella
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Dept Genet Epidemiol Psychiat, Mannheim, Germany..
    Spanagel, Rainer
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Inst Psychopharmacol, Mannheim, Germany..
    Witt, Stephanie H.
    Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Dept Genet Epidemiol Psychiat, Mannheim, Germany.;Heidelberg Univ, Med Fac Mannheim, Ctr Innovat Psychiat & Psychotherapeut Res, Cent Inst Mental Hlth,Biobank, Mannheim, Germany..
    Multi-omics signatures of alcohol use disorder in the dorsal and ventral striatum2022In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 12, no 1, article id 190Article in journal (Refereed)
    Abstract [en]

    Alcohol Use Disorder (AUD) is a major contributor to global mortality and morbidity. Postmortem human brain tissue enables the investigation of molecular mechanisms of AUD in the neurocircuitry of addiction. We aimed to identify differentially expressed (DE) genes in the ventral and dorsal striatum between individuals with AUD and controls, and to integrate the results with findings from genome- and epigenome-wide association studies (GWAS/EWAS) to identify functionally relevant molecular mechanisms of AUD. DNA-methylation and gene expression (RNA-seq) data was generated from postmortem brain samples of 48 individuals with AUD and 51 controls from the ventral striatum (VS) and the dorsal striatal regions caudate nucleus (CN) and putamen (PUT). We identified DE genes using DESeq2, performed gene-set enrichment analysis (GSEA), and tested enrichment of DE genes in results of GWASs using MAGMA. Weighted correlation network analysis (WGCNA) was performed for DNA-methylation and gene expression data and gene overlap was tested. Differential gene expression was observed in the dorsal (FDR < 0.05), but not the ventral striatum of AUD cases. In the VS, DE genes at FDR < 0.25 were overrepresented in a recent GWAS of problematic alcohol use. The ARHGEF15 gene was upregulated in all three brain regions. GSEA in CN and VS pointed towards cell-structure associated GO-terms and in PUT towards immune pathways. The WGCNA modules most strongly associated with AUD showed strong enrichment for immune response and inflammation pathways. Our integrated analysis of multi-omics data sets provides further evidence for the importance of immune- and inflammation-related processes in AUD.

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  • 156.
    Zuffa, Simone
    et al.
    Imperial Coll London, Fac Med, Dept Metab Digest & Reprod, London SW7 2AZ, England..
    Schimmel, Patrick
    Wageningen Univ, Lab Microbiol, Wageningen, Netherlands..
    Gonzalez-Santana, Ayoze
    Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden..
    Belzer, Clara
    Wageningen Univ, Lab Microbiol, Wageningen, Netherlands..
    Knol, Jan
    Wageningen Univ, Lab Microbiol, Wageningen, Netherlands.;Danone Nutr Res, Uppsalalaan 12, NL-3584 CT Utrecht, Netherlands..
    Bolte, Sven
    Ctr Psychiat Res, Ctr Neurodev Disorders KIND, Stockholm, Sweden.;Karolinska Inst, Dept Womens & Childrens Hlth, Stockholm, Sweden.;Reg Stockholm, Stockholm Hlth Care Serv, Stockholm, Sweden.;Reg Stockholm, Stockholm Hlth Care Serv, Child & Adolescent Psychiat, Stockholm, Sweden.;Curtin Univ, Curtin Sch Allied Hlth, Curtin Autism Res Grp, Perth, WA, Australia..
    Falck-Ytter, Terje
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Psychology. Ctr Psychiat Res, Ctr Neurodev Disorders KIND, Stockholm, Sweden.;Karolinska Inst, Dept Womens & Childrens Hlth, Stockholm, Sweden.;Reg Stockholm, Stockholm Hlth Care Serv, Stockholm, Sweden..
    Forssberg, Hans
    Karolinska Inst, Dept Womens & Childrens Hlth, Stockholm, Sweden..
    Swann, Jonathan
    Imperial Coll London, Fac Med, Dept Metab Digest & Reprod, London SW7 2AZ, England.;Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden.;Univ Southampton, Fac Med, Sch Human Dev & Hlth, Univ Rd, Southampton SO17 1BJ, England..
    Heijtz, Rochellys Diaz
    Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden..
    Early-life differences in the gut microbiota composition and functionality of infants at elevated likelihood of developing autism spectrum disorder2023In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 13, article id 257Article in journal (Refereed)
    Abstract [en]

    Evidence from cross-sectional human studies, and preliminary microbial-based intervention studies, have implicated the microbiota-gut-brain axis in the neurobiology of autism spectrum disorder (ASD). Using a prospective longitudinal study design, we investigated the developmental profile of the fecal microbiota and metabolome in infants with (n = 16) and without (n = 19) a family history of ASD across the first 36 months of life. In addition, the general developmental levels of infants were evaluated using the Mullen Scales of Early Learning (MSEL) test at 5 and 36 months of age, and with ADOS-2 at 36 months of age. At 5 months of age, infants at elevated-likelihood of ASD (EL) harbored less Bifidobacterium and more Clostridium and Klebsiella species compared to the low-likelihood infants (LL). Untargeted metabolic profiling highlighted that LL infants excreted a greater amount of fecal & gamma;-aminobutyric acid (GABA) at 5 months, which progressively declined with age. Similar age-dependent patterns were not observed in the EL group, with GABA being consistently low across all timepoints. Integrated microbiome-metabolome analysis showed a positive correlation between GABA and Bifidobacterium species and negative associations with Clostridium species. In vitro experiments supported these observations demonstrating that bifidobacteria can produce GABA while clostridia can consume it. At the behavioral level, there were no significant differences between the EL and LL groups at 5 months. However, at 36 months of age, the EL group had significantly lower MSEL and ADOS-2 scores compared to the LL group. Taken together, the present results reveal early life alterations in gut microbiota composition and functionality in infants at elevated-likelihood of ASD. These changes occur before any behavioral impairments can be detected, supporting a possible role for the gut microbiota in emerging behavioral variability later in life.

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  • 157.
    Ågren, Thomas
    et al.
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Psychology.
    Furmark, Tomas
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Psychology.
    Eriksson, Elias
    Sektionen för farmakologi, Göteborgs universitet.
    Fredrikson, Mats
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Psychology.
    Human fear reconsolidation and allelic differences in serotonergic and dopaminergic genes2012In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 2, article id e76Article in journal (Refereed)
    Abstract [en]

    Fear memory persistence, central for the development and maintenance of anxiety disorders, is partially genetically controlled. Recently, consolidation and reconsolidation processes have been reported to affect fear memory stability and integrity. This study explored the impact of reconsolidation processes and genetic make-up on fear reacquisition by manipulating reconsolidation using extinction performed outside or inside a reconsolidation interval. Reacquisition measured by skin conductance responses was stronger in individuals that extinguished outside (6 h) than inside (10 min) the reconsolidation interval. However, the effect was predominantly present in val/val homozygotes of the functional val158met polymorphism of the Catechol O-methyltransferase (COMT) enzyme and in short allele carriers of the serotonin transporter length 5-HTTLPR polymorphism. These results demonstrate that reconsolidation of human fear memory is influenced by dopamine and serotonin related genes.

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