Genome-wide association study of Alzheimer's disease with psychotic symptoms
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 unde...
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| Published in | Molecular psychiatry Vol. 17; no. 12; pp. 1316 - 1327 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.12.2012
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| 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. |
|---|---|
| AbstractList | 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.Inall,1299AD 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 x [10.sup.-7];'AD + PvControls' P = 1.11 x [10.sup.-4]). SNPs upstream of SLC2A9 (rs6834555, P = 3.0 x [10.sup.-7])and within VSNL1 (rs4038131, P = 5.9 x [10.sup.-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. 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.Inall,1299AD 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 x [10.sup.-7];'AD + PvControls' P = 1.11 x [10.sup.-4]). SNPs upstream of SLC2A9 (rs6834555, P = 3.0 x [10.sup.-7])and within VSNL1 (rs4038131, P = 5.9 x [10.sup.-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. Molecular Psychiatry (2012) 17, 1316-1327; doi: 10.1038/mp.2011.125; published online 18 October 2011 Keywords: Alzheimer's disease; psychosis; behavioural symptoms; genome-wide association study; genetic 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.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. 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. Psychotic symptoms occur in approximately 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 (GWAS) to identify loci that a) increase susceptibility to an AD and subsequent psychotic symptoms; or b) modify risk of psychotic symptoms in the presence of neurodegeneration caused by AD. 1299 AD cases with psychosis (AD+P), 735 AD cases without psychosis (AD−P) and 5659 controls were drawn from GERAD1, the NIA-LOAD family study and the University of Pittsburgh ADRC GWAS. Unobserved genotypes were imputed to provide data on > 1.8 million SNPs. Analyses in each dataset were completed comparing a) AD+P to AD−P cases, and b) AD+P cases with controls (GERAD1, ADRC only). Aside from the 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 to controls. These findings warrant further investigation in larger, appropriately powered samples in which the presence of psychotic symptoms in AD has been well characterised. 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. Psychotic symptoms occur in approximately 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 (GWAS) to identify loci that a) increase susceptibility to an AD and subsequent psychotic symptoms; or b) modify risk of psychotic symptoms in the presence of neurodegeneration caused by AD. 1299 AD cases with psychosis (AD+P), 735 AD cases without psychosis (AD-P) and 5659 controls were drawn from GERAD1, the NIA-LOAD family study and the University of Pittsburgh ADRC GWAS. Unobserved genotypes were imputed to provide data on > 1.8 million SNPs. Analyses in each dataset were completed comparing a) AD+P to AD-P cases, and b) AD+P cases with controls (GERAD1, ADRC only). Aside from the APOE locus, the strongest evidence for association was observed in an intergenic region on chromosome 4 (rs753129; 'AD+PvAD-P' P=2.85 x 10-7; 'AD+PvControls' P=1.11 x 10-4). SNPs upstream of SLC2A9 (rs6834555, P=3.0x10-7) and within VSNL1 (rs4038131, P=5.9x10-7) showed strongest evidence for association with AD+P when compared to controls. These findings warrant further investigation in larger, appropriately powered samples in which the presence of psychotic symptoms in AD has been well characterised. Psychotic symptoms occur in similar to 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 super(-7); 'AD+PvControls' P=1.11 10 super(-4)). SNPs upstream of SLC2A9 (rs6834555, P=3.0 10 super(-7)) and within VSNL1 (rs4038131, P=5.9 10 super(-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. 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. |
| Audience | Academic |
| Author | Jones, N Passmore, P Jones, L Lynch, A Sims, R DeKosky, S T Priotsi, P Demirci, F Y Stretton, A Gurling, H Barmada, M M Lovestone, S Brayne, C Livingston, G Gerrish, A Lopez, O L Russo, G McQuillin, A Ivanov, D Abraham, R Mayeux, R Owen, M J Harold, D Johnston, J Lawlor, B Moskvina, V Sweet, R Chapman, J Kamboh, M I Klei, L O'Donovan, M C Hollingworth, P Craig, D McGuinness, B Lupton, M Bass, N J Williams, J Devlin, B Gill, M Holmans, P Holmes, C |
| AuthorAffiliation | 2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213, USA 3 Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213, USA 6 Institute of Public Health, University of Cambridge, Cambridge, UK 15 University of Virginia School of Medicine, Charlottesville VA, 22908 USA 13 Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA 5 Department of Neuroscience, Institute of Psychiatry, Kings College, London, UK 14 Taub Institute and the Department of Neurology, Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032, USA 7 Mercer's Institute for Research on Aging, St. James Hospital and Trinity College, Dublin, Ireland 10 Department of Mental Health Sciences, University College London, UK 8 Ageing Group, Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen's University of Belfast, UK 9 D |
| AuthorAffiliation_xml | – name: 8 Ageing Group, Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen's University of Belfast, UK – name: 1 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 – name: 2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213, USA – name: 10 Department of Mental Health Sciences, University College London, UK – name: 15 University of Virginia School of Medicine, Charlottesville VA, 22908 USA – name: 14 Taub Institute and the Department of Neurology, Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032, USA – name: 4 VISN 4 Mental Illness Research, Education and Clinical Center (MIRECC), VA Pittsburgh Healthcare System, Pittsburgh, PA, 15206 USA – name: 7 Mercer's Institute for Research on Aging, St. James Hospital and Trinity College, Dublin, Ireland – name: 6 Institute of Public Health, University of Cambridge, Cambridge, UK – name: 5 Department of Neuroscience, Institute of Psychiatry, Kings College, London, UK – name: 9 Division of Clinical Neurosciences, School of Medicine, University of Southampton, Southampton, UK – name: 13 Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA – name: 3 Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213, USA |
| Author_xml | – sequence: 1 givenname: P surname: Hollingworth fullname: Hollingworth, P organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 2 givenname: R surname: Sweet fullname: Sweet, R email: SweetRA@upmc.edu organization: Department of Psychiatry, University of Pittsburgh, School of Medicine, Department of Neurology, University of Pittsburgh, School of Medicine, VISN 4 Mental Illness Research, Education and Clinical Center (MIRECC), VA Pittsburgh Healthcare System – sequence: 3 givenname: R surname: Sims fullname: Sims, R organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 4 givenname: D surname: Harold fullname: Harold, D organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 5 givenname: G surname: Russo fullname: Russo, G organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 6 givenname: R surname: Abraham fullname: Abraham, R organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 7 givenname: A surname: Stretton fullname: Stretton, A organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 8 givenname: N surname: Jones fullname: Jones, N organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 9 givenname: A surname: Gerrish fullname: Gerrish, A organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 10 givenname: J surname: Chapman fullname: Chapman, J organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 11 givenname: D surname: Ivanov fullname: Ivanov, D organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 12 givenname: V surname: Moskvina fullname: Moskvina, V organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 13 givenname: S surname: Lovestone fullname: Lovestone, S organization: Department of Neuroscience, Kings College London, Institute of Psychiatry – sequence: 14 givenname: P surname: Priotsi fullname: Priotsi, P organization: Department of Neuroscience, Kings College London, Institute of Psychiatry – sequence: 15 givenname: M surname: Lupton fullname: Lupton, M organization: Department of Neuroscience, Kings College London, Institute of Psychiatry – sequence: 16 givenname: C surname: Brayne fullname: Brayne, C organization: Institute of Public Health, University of Cambridge – sequence: 17 givenname: M surname: Gill fullname: Gill, M organization: Mercer's Institute for Research on Aging, St James Hospital and Trinity College – sequence: 18 givenname: B surname: Lawlor fullname: Lawlor, B organization: Mercer's Institute for Research on Aging, St James Hospital and Trinity College – sequence: 19 givenname: A surname: Lynch fullname: Lynch, A organization: Mercer's Institute for Research on Aging, St James Hospital and Trinity College – sequence: 20 givenname: D surname: Craig fullname: Craig, D organization: Ageing Group, Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen's University of Belfast – sequence: 21 givenname: B surname: McGuinness fullname: McGuinness, B organization: Ageing Group, Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen's University of Belfast – sequence: 22 givenname: J surname: Johnston fullname: Johnston, J organization: Ageing Group, Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen's University of Belfast – sequence: 23 givenname: C surname: Holmes fullname: Holmes, C organization: Division of Clinical Neurosciences, School of Medicine, University of Southampton – sequence: 24 givenname: G surname: Livingston fullname: Livingston, G organization: Department of Mental Health Sciences, University College London – sequence: 25 givenname: N J surname: Bass fullname: Bass, N J organization: Department of Mental Health Sciences, University College London – sequence: 26 givenname: H surname: Gurling fullname: Gurling, H organization: Department of Mental Health Sciences, University College London – sequence: 27 givenname: A surname: McQuillin fullname: McQuillin, A organization: Department of Mental Health Sciences, University College London – sequence: 30 givenname: P surname: Holmans fullname: Holmans, P organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 31 givenname: L surname: Jones fullname: Jones, L organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 32 givenname: B surname: Devlin fullname: Devlin, B organization: Department of Psychiatry, University of Pittsburgh, School of Medicine – sequence: 33 givenname: L surname: Klei fullname: Klei, L organization: Department of Psychiatry, University of Pittsburgh, School of Medicine – sequence: 34 givenname: M M surname: Barmada fullname: Barmada, M M organization: Taub Institute and the Department of Neurology, Columbia University, College of Physicians and Surgeons – sequence: 35 givenname: F Y surname: Demirci fullname: Demirci, F Y organization: Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh – sequence: 36 givenname: S T surname: DeKosky fullname: DeKosky, S T organization: Department of Neurology, University of Pittsburgh, School of Medicine, University of Virginia School of Medicine – sequence: 37 givenname: O L surname: Lopez fullname: Lopez, O L organization: Department of Neurology, University of Pittsburgh, School of Medicine – sequence: 38 givenname: P surname: Passmore fullname: Passmore, P organization: Ageing Group, Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen's University of Belfast – sequence: 39 givenname: M J surname: Owen fullname: Owen, M J organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 40 givenname: M C surname: O'Donovan fullname: O'Donovan, M C organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University – sequence: 41 givenname: R surname: Mayeux fullname: Mayeux, R organization: Taub Institute and the Department of Neurology, Columbia University, College of Physicians and Surgeons – sequence: 42 givenname: M I surname: Kamboh fullname: Kamboh, M I organization: Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh – sequence: 43 givenname: J surname: Williams fullname: Williams, J email: williamsj@cardiff.ac.uk organization: Department of Psychological Medicine and Neurology, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Neurosciences and Mental Health Research Institute, School of Medicine, Cardiff University |
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| ContentType | Journal Article |
| Contributor | Gaskel, Peter Morgan, Kevin Heuser, Isabella Hyman, Bradley T Rossor, Martin Kornhuber, Johannes Sims, Rebecca Gurling, Hugh Moskvina, Valentina Collinge, John Williamson, Jennifer Heun, Reiner Kowall, Neil Fox, Nick Mead, Simon Green, Robert Wiltfang, Jens Hamshere, Marian Mühleisen, Thomas W O'Donovan, Michael Morris, John C Maier, Wolfgang Moebus, Susanne Shaw, Christopher E Nöthen, Markus M Thomas, Charlene Gwilliam, Rhian Morgan, Angharad Bass, Nicholas J Dowzell, Kimberley Schmechel, Donald Hampel, Harald Owen, Michael J Carrasquillo, Minerva M Kuntz, Karen Lupton, Michelle K Kölsch, Heike Dichgans, Martin Guerreiro, Rita Mayo, Kevin Hüll, Michael Blacker, Deborah Wichmann, H-Erich Brown, Kristelle Klopp, Norman McGuinness, Bernadette Rujescu, Dan Goate, Alison Younkin, Steven G Hardy, John Growdon, John H Holmans, Peter Cruchaga, Carlos Nowotny, Petra van den Bussche, Hendrik Farlow, Martin R Boeve, Bradley Proitsi, Petroula Passmore, Peter Santana, Vincent Farrer, Lindsay Powell, John Jones, Nicola Horner, Kelly Lawlor, Brian Lynch, Aoibhinn |
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| Copyright | Macmillan Publishers Limited 2012 2015 INIST-CNRS COPYRIGHT 2012 Nature Publishing Group Copyright Nature Publishing Group Dec 2012 Macmillan Publishers Limited 2012. Distributed under a Creative Commons Attribution 4.0 International License |
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| Keywords | genetic behavioural symptoms Alzheimer's disease psychosis genome-wide association study Nervous system diseases Alzheimer disease Cerebral disorder Behavioral disorder Psychosis Symptomatology Central nervous system disease Genetics Degenerative disease |
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| Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 These authors contributed equally to this work 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. 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. |
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| PublicationTitle | Molecular psychiatry |
| PublicationTitleAbbrev | Mol Psychiatry |
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| PublicationYear | 2012 |
| Publisher | Nature Publishing Group UK Nature Publishing Group |
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62 A Biffi (BFmp2011125_CR7) 2010; 67 B Devlin (BFmp2011125_CR44) 1999; 55 GL Bowman (BFmp2011125_CR59) 2010; 19 G Jun (BFmp2011125_CR6) 2010; 67 JL Cummings (BFmp2011125_CR31) 1994; 44 L Berg (BFmp2011125_CR37) 1988; 24 BM Schjeide (BFmp2011125_CR72) 2011; 68 D Harold (BFmp2011125_CR2) 2009; 41 S Cichon (BFmp2011125_CR50) 2011; 88 MC O’Donovan (BFmp2011125_CR12) 2009; 126 MA DeMichele-Sweet (BFmp2011125_CR22) 2010; 19 RA Sweet (BFmp2011125_CR19) 2002; 58 SS Mirra (BFmp2011125_CR26) 1991; 41 KH Braunewell (BFmp2011125_CR53) 2009; 335 MC O’Donovan (BFmp2011125_CR47) 2008; 40 AD Rule (BFmp2011125_CR57) 2011; 50 P Hollingworth (BFmp2011125_CR1) 2011; 26 N Craddock (BFmp2011125_CR69) 2009; 35 AL Price (BFmp2011125_CR40) 2006; 38 RA Sweet (BFmp2011125_CR21) 2010; 133 MA Demichele-Sweet (BFmp2011125_CR24) 2011; 32 MA Demichele-Sweet (BFmp2011125_CR64) 2011; 2011 PN Tariot (BFmp2011125_CR33) 1995; 152 EM Wijsman (BFmp2011125_CR23) 2011; 7 BFmp2011125_CR39 G Lettre (BFmp2011125_CR68) 2008; 17 P Lichtenstein (BFmp2011125_CR66) 2009; 373 P Hollingworth (BFmp2011125_CR18) 2007; 144B V Vitart (BFmp2011125_CR58) 2008; 40 H Stefansson (BFmp2011125_CR46) 2009; 460 JM Lee (BFmp2011125_CR54) 2008; 54 AC Naj (BFmp2011125_CR10) 2011; 43 |
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| Snippet | Psychotic symptoms occur in ∼40% of subjects with Alzheimer's disease (AD) and are associated with more rapid cognitive decline and increased functional... Psychotic symptoms occur in ~40% of subjects with Alzheimer's disease (AD) and are associated with more rapid cognitive decline and increased functional... Psychotic symptoms occur in similar to 40% of subjects with Alzheimer's disease (AD) and are associated with more rapid cognitive decline and increased... Psychotic symptoms occur in approximately 40% of subjects with Alzheimer's disease (AD) and are associated with more rapid cognitive decline and increased... Psychotic symptoms occur in approximately 40% of subjects with Alzheimer’s disease (AD) and are associated with more rapid cognitive decline and increased... |
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| SubjectTerms | 631/208/205/2138 631/378/1689/1761 692/699/375/132/1283 Adult and adolescent clinical studies Aged Aged, 80 and over Aging Alzheimer Disease - complications Alzheimer Disease - genetics Alzheimer Disease - psychology Alzheimer's disease Apolipoprotein E Apolipoproteins E - genetics Behavioral Sciences Biological and medical sciences Biological Psychology Bipolar disorder Case-Control Studies Chromosome 4 Chromosomes, Human, Pair 4 - genetics Cognitive ability Consortia Data processing Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Development and progression Disease DNA, Intergenic - genetics Family studies Female Gene mapping Genes Genetic aspects Genetic Predisposition to Disease - genetics Genetics Genome-wide association studies Genome-Wide Association Study - methods Genome-Wide Association Study - statistics & numerical data Genomes Genomics Glucose Transport Proteins, Facilitative - genetics Heritability Human health and pathology Humans Life Sciences Male Medical sciences Medicine Medicine & Public Health Mental disorders Mental health Middle Aged Neurocalcin - genetics Neurodegeneration Neurodegenerative diseases Neurology Neurosciences Organic mental disorders. Neuropsychology original-article Pharmacotherapy Physiological aspects Polymorphism, Single Nucleotide - genetics Proteins Psychiatric Status Rating Scales - statistics & numerical data Psychiatrics and mental health Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Psychosis Psychotic Disorders - complications Psychotic Disorders - diagnosis Psychotic Disorders - genetics Public health Single-nucleotide polymorphism |
| Title | Genome-wide association study of Alzheimer's disease with psychotic symptoms |
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