Genome-wide Association Study of Alzheimer’s disease with Psychotic Symptoms View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-10-18

AUTHORS

Paul Hollingworth, Robert Sweet, Rebecca Sims, Denise Harold, Giancarlo Russo, Richard Abraham, Alexandra Stretton, Nicola Jones, Amy Gerrish, Jade Chapman, Dobril Ivanov, Valentina Moskvina, Simon Lovestone, Petroula Priotsi, Michelle Lupton, Carol Brayne, Michael Gill, Brian Lawlor, Aoibhinn Lynch, David Craig, Bernadette McGuinness, Janet Johnston, Clive Holmes, Gill Livingston, Nicholas J. Bass, Hugh Gurling, Andrew McQuillin, , , Peter Holmans, Lesley Jones, Bernie Devlin, Lambertus Klei, M. Michael Barmada, F. Yesim Demirci, Steven T. DeKosky, Oscar L. Lopez, Peter Passmore, Michael J Owen, Michael C O’Donovan, Richard Mayeux, M. Ilyas Kamboh, Julie Williams

ABSTRACT

Psychotic symptoms occur in ~40% of subjects with Alzheimer's disease (AD) and are associated with more rapid cognitive decline and increased functional deficits. They show heritability up to 61% and have been proposed as a marker for a disease subtype suitable for gene mapping efforts. We undertook a combined analysis of three genome-wide association studies (GWASs) to identify loci that (1) increase susceptibility to an AD and subsequent psychotic symptoms; or (2) modify risk of psychotic symptoms in the presence of neurodegeneration caused by AD. In all, 1299 AD cases with psychosis (AD+P), 735 AD cases without psychosis (AD-P) and 5659 controls were drawn from Genetic and Environmental Risk in AD Consortium 1 (GERAD1), the National Institute on Aging Late-Onset Alzheimer's Disease (NIA-LOAD) family study and the University of Pittsburgh Alzheimer Disease Research Center (ADRC) GWASs. Unobserved genotypes were imputed to provide data on >1.8 million single-nucleotide polymorphisms (SNPs). Analyses in each data set were completed comparing (1) AD+P to AD-P cases, and (2) AD+P cases with controls (GERAD1, ADRC only). Aside from the apolipoprotein E (APOE) locus, the strongest evidence for association was observed in an intergenic region on chromosome 4 (rs753129; 'AD+PvAD-P' P=2.85 × 10(-7); 'AD+PvControls' P=1.11 × 10(-4)). SNPs upstream of SLC2A9 (rs6834555, P=3.0 × 10(-7)) and within VSNL1 (rs4038131, P=5.9 × 10(-7)) showed strongest evidence for association with AD+P when compared with controls. These findings warrant further investigation in larger, appropriately powered samples in which the presence of psychotic symptoms in AD has been well characterized. More... »

PAGES

1316-1327

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  • Journal

    TITLE

    Molecular Psychiatry

    ISSUE

    12

    VOLUME

    17

    Author Affiliations

  • Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, Department of Psychological Medicine and Neurology, School of Medicine, Cardiff University, Cardiff, UK
  • VISN 4 Mental Illness Research, Education and Clinical Center (MIRECC), VA Pittsburgh Healthcare System, Pittsburgh, PA, 15206 USA
  • Department of Neuroscience, Institute of Psychiatry, Kings College, London, UK
  • Institute of Public Health, University of Cambridge, Cambridge, UK
  • Mercer’s Institute for Research on Aging, St. James Hospital and Trinity College, Dublin, Ireland
  • Ageing Group, Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen’s University of Belfast, UK
  • Division of Clinical Neurosciences, School of Medicine, University of Southampton, Southampton, UK
  • Department of Mental Health Sciences, University College London, UK
  • Data used in the preparation of this article were obtained from the Genetic and Environmental Risk in Alzheimer’s disease GWAS (GERAD) genome-wide association study(2). As such, the investigators within the GERAD consortium contributed to the design and implementation of GERAD and/or provided data but did not participate in analysis or writing of this report. See supplementary content, for members of the GERAD consortium
  • Data used in the preparation of this article were obtained from the National Institute on Aging Late-Onset Alzheimer’s disease Family Study Group (NIA-LOAD). As such, the investigators within the NIA-LOAD consortium contributed to the design and implementation of NIA-LOAD and/or provided data but did not participate in analysis or writing of this report. See supplementary content, for members of the NIA-LOAD consortium
  • Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213, USA
  • Taub Institute and the Department of Neurology , Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032, USA
  • Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA
  • University of Virginia School of Medicine, Charlottesville VA, 22908 USA
  • Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213, USA
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/mp.2011.125

    DOI

    http://dx.doi.org/10.1038/mp.2011.125

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1038988701

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/22005930


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