Cooperative Genome-Wide Analysis Shows Increased Homozygosity in Early Onset Parkinson's Disease
Parkinson's disease (PD) occurs in both familial and sporadic forms, and both monogenic and complex genetic factors have been identified. Early onset PD (EOPD) is particularly associated with autosomal recessive (AR) mutations, and three genes, PARK2, PARK7 and PINK1, have been found to carry m...
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| Vydáno v: | PloS one Ročník 7; číslo 3; s. e28787 |
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| Hlavní autoři: | , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
Public Library of Science
12.03.2012
Public Library of Science (PLoS) |
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| ISSN: | 1932-6203, 1932-6203 |
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| Abstract | Parkinson's disease (PD) occurs in both familial and sporadic forms, and both monogenic and complex genetic factors have been identified. Early onset PD (EOPD) is particularly associated with autosomal recessive (AR) mutations, and three genes, PARK2, PARK7 and PINK1, have been found to carry mutations leading to AR disease. Since mutations in these genes account for less than 10% of EOPD patients, we hypothesized that further recessive genetic factors are involved in this disorder, which may appear in extended runs of homozygosity.We carried out genome wide SNP genotyping to look for extended runs of homozygosity (ROHs) in 1,445 EOPD cases and 6,987 controls. Logistic regression analyses showed an increased level of genomic homozygosity in EOPD cases compared to controls. These differences are larger for ROH of 9 Mb and above, where there is a more than three-fold increase in the proportion of cases carrying a ROH. These differences are not explained by occult recessive mutations at existing loci. Controlling for genome wide homozygosity in logistic regression analyses increased the differences between cases and controls, indicating that in EOPD cases ROHs do not simply relate to genome wide measures of inbreeding. Homozygosity at a locus on chromosome19p13.3 was identified as being more common in EOPD cases as compared to controls. Sequencing analysis of genes and predicted transcripts within this locus failed to identify a novel mutation causing EOPD in our cohort.There is an increased rate of genome wide homozygosity in EOPD, as measured by an increase in ROHs. These ROHs are a signature of inbreeding and do not necessarily harbour disease-causing genetic variants. Although there might be other regions of interest apart from chromosome 19p13.3, we lack the power to detect them with this analysis. |
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| AbstractList | Parkinson's disease (PD) occurs in both familial and sporadic forms, and both monogenic and complex genetic factors have been identified. Early onset PD (EOPD) is particularly associated with autosomal recessive (AR) mutations, and three genes, PARK2, PARK7 and PINK1, have been found to carry mutations leading to AR disease. Since mutations in these genes account for less than 10% of EOPD patients, we hypothesized that further recessive genetic factors are involved in this disorder, which may appear in extended runs of homozygosity. We carried out genome wide SNP genotyping to look for extended runs of homozygosity (ROHs) in 1,445 EOPD cases and 6,987 controls. Logistic regression analyses showed an increased level of genomic homozygosity in EOPD cases compared to controls. These differences are larger for ROH of 9 Mb and above, where there is a more than three-fold increase in the proportion of cases carrying a ROH. These differences are not explained by occult recessive mutations at existing loci. Controlling for genome wide homozygosity in logistic regression analyses increased the differences between cases and controls, indicating that in EOPD cases ROHs do not simply relate to genome wide measures of inbreeding. Homozygosity at a locus on chromosome19p13.3 was identified as being more common in EOPD cases as compared to controls. Sequencing analysis of genes and predicted transcripts within this locus failed to identify a novel mutation causing EOPD in our cohort. There is an increased rate of genome wide homozygosity in EOPD, as measured by an increase in ROHs. These ROHs are a signature of inbreeding and do not necessarily harbour disease-causing genetic variants. Although there might be other regions of interest apart from chromosome 19p13.3, we lack the power to detect them with this analysis. Parkinson's disease (PD) occurs in both familial and sporadic forms, and both monogenic and complex genetic factors have been identified. Early onset PD (EOPD) is particularly associated with autosomal recessive (AR) mutations, and three genes, PARK2, PARK7 and PINK1, have been found to carry mutations leading to AR disease. Since mutations in these genes account for less than 10% of EOPD patients, we hypothesized that further recessive genetic factors are involved in this disorder, which may appear in extended runs of homozygosity. We carried out genome wide SNP genotyping to look for extended runs of homozygosity (ROHs) in 1,445 EOPD cases and 6,987 controls. Logistic regression analyses showed an increased level of genomic homozygosity in EOPD cases compared to controls. These differences are larger for ROH of 9 Mb and above, where there is a more than three-fold increase in the proportion of cases carrying a ROH. These differences are not explained by occult recessive mutations at existing loci. Controlling for genome wide homozygosity in logistic regression analyses increased the differences between cases and controls, indicating that in EOPD cases ROHs do not simply relate to genome wide measures of inbreeding. Homozygosity at a locus on chromosome19p13.3 was identified as being more common in EOPD cases as compared to controls. Sequencing analysis of genes and predicted transcripts within this locus failed to identify a novel mutation causing EOPD in our cohort. There is an increased rate of genome wide homozygosity in EOPD, as measured by an increase in ROHs. These ROHs are a signature of inbreeding and do not necessarily harbour disease-causing genetic variants. Although there might be other regions of interest apart from chromosome 19p13.3, we lack the power to detect them with this analysis. Parkinson's disease (PD) occurs in both familial and sporadic forms, and both monogenic and complex genetic factors have been identified. Early onset PD (EOPD) is particularly associated with autosomal recessive (AR) mutations, and three genes, PARK2, PARK7 and PINK1, have been found to carry mutations leading to AR disease. Since mutations in these genes account for less than 10% of EOPD patients, we hypothesized that further recessive genetic factors are involved in this disorder, which may appear in extended runs of homozygosity. Parkinson's disease (PD) occurs in both familial and sporadic forms, and both monogenic and complex genetic factors have been identified. Early onset PD (EOPD) is particularly associated with autosomal recessive (AR) mutations, and three genes, PARK2, PARK7 and PINK1, have been found to carry mutations leading to AR disease. Since mutations in these genes account for less than 10% of EOPD patients, we hypothesized that further recessive genetic factors are involved in this disorder, which may appear in extended runs of homozygosity.We carried out genome wide SNP genotyping to look for extended runs of homozygosity (ROHs) in 1,445 EOPD cases and 6,987 controls. Logistic regression analyses showed an increased level of genomic homozygosity in EOPD cases compared to controls. These differences are larger for ROH of 9 Mb and above, where there is a more than three-fold increase in the proportion of cases carrying a ROH. These differences are not explained by occult recessive mutations at existing loci. Controlling for genome wide homozygosity in logistic regression analyses increased the differences between cases and controls, indicating that in EOPD cases ROHs do not simply relate to genome wide measures of inbreeding. Homozygosity at a locus on chromosome19p13.3 was identified as being more common in EOPD cases as compared to controls. Sequencing analysis of genes and predicted transcripts within this locus failed to identify a novel mutation causing EOPD in our cohort.There is an increased rate of genome wide homozygosity in EOPD, as measured by an increase in ROHs. These ROHs are a signature of inbreeding and do not necessarily harbour disease-causing genetic variants. Although there might be other regions of interest apart from chromosome 19p13.3, we lack the power to detect them with this analysis.Parkinson's disease (PD) occurs in both familial and sporadic forms, and both monogenic and complex genetic factors have been identified. Early onset PD (EOPD) is particularly associated with autosomal recessive (AR) mutations, and three genes, PARK2, PARK7 and PINK1, have been found to carry mutations leading to AR disease. Since mutations in these genes account for less than 10% of EOPD patients, we hypothesized that further recessive genetic factors are involved in this disorder, which may appear in extended runs of homozygosity.We carried out genome wide SNP genotyping to look for extended runs of homozygosity (ROHs) in 1,445 EOPD cases and 6,987 controls. Logistic regression analyses showed an increased level of genomic homozygosity in EOPD cases compared to controls. These differences are larger for ROH of 9 Mb and above, where there is a more than three-fold increase in the proportion of cases carrying a ROH. These differences are not explained by occult recessive mutations at existing loci. Controlling for genome wide homozygosity in logistic regression analyses increased the differences between cases and controls, indicating that in EOPD cases ROHs do not simply relate to genome wide measures of inbreeding. Homozygosity at a locus on chromosome19p13.3 was identified as being more common in EOPD cases as compared to controls. Sequencing analysis of genes and predicted transcripts within this locus failed to identify a novel mutation causing EOPD in our cohort.There is an increased rate of genome wide homozygosity in EOPD, as measured by an increase in ROHs. These ROHs are a signature of inbreeding and do not necessarily harbour disease-causing genetic variants. Although there might be other regions of interest apart from chromosome 19p13.3, we lack the power to detect them with this analysis. |
| Audience | Academic |
| Author | Heutink, Peter Wood, Nicholas W. Morris, Huw R. Brice, Alexis Hardy, John Martinez, Maria Holmans, Peter Simón-Sánchez, Javier Nalls, Michael A. Kilarski, Laura L. Williams, Nigel Schulte, Claudia Gasser, Thomas Singleton, Andrew B. |
| AuthorAffiliation | 8 Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom 4 Inserm, UMR 1043, Toulouse, France 6 Department of Psychological Medicine & Neurology, Cardiff University School of Medicine, Cardiff, United Kingdom 10 Inserm, U975, Paris, France 2 MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University School of Medicine, Cardiff, United Kingdom University of Florida, United States of America 1 Section of Medical Genomics, Department of Clinical Genetics, VU University Medical Centre, Amsterdam, The Netherlands 3 Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, United States of America 5 Paul Sabatier University, Toulouse, France 7 Department for Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research, and DZNE, German Center for Neurodegenerative Diseases, Tübingen, Germany 11 Cnrs, UMR 7225, Paris, France 9 Université Pierre et Marie Curie-Paris6, Centre de Recherche de l'I |
| AuthorAffiliation_xml | – name: University of Florida, United States of America – name: 4 Inserm, UMR 1043, Toulouse, France – name: 1 Section of Medical Genomics, Department of Clinical Genetics, VU University Medical Centre, Amsterdam, The Netherlands – name: 11 Cnrs, UMR 7225, Paris, France – name: 9 Université Pierre et Marie Curie-Paris6, Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, UMR-S975, Paris, France – name: 8 Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom – name: 3 Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, United States of America – name: 6 Department of Psychological Medicine & Neurology, Cardiff University School of Medicine, Cardiff, United Kingdom – name: 5 Paul Sabatier University, Toulouse, France – name: 7 Department for Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research, and DZNE, German Center for Neurodegenerative Diseases, Tübingen, Germany – name: 2 MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University School of Medicine, Cardiff, United Kingdom – name: 10 Inserm, U975, Paris, France |
| Author_xml | – sequence: 1 givenname: Javier surname: Simón-Sánchez fullname: Simón-Sánchez, Javier – sequence: 2 givenname: Laura L. surname: Kilarski fullname: Kilarski, Laura L. – sequence: 3 givenname: Michael A. surname: Nalls fullname: Nalls, Michael A. – sequence: 4 givenname: Maria surname: Martinez fullname: Martinez, Maria – sequence: 5 givenname: Claudia surname: Schulte fullname: Schulte, Claudia – sequence: 6 givenname: Peter surname: Holmans fullname: Holmans, Peter – sequence: 7 givenname: Thomas surname: Gasser fullname: Gasser, Thomas – sequence: 8 givenname: John surname: Hardy fullname: Hardy, John – sequence: 9 givenname: Andrew B. surname: Singleton fullname: Singleton, Andrew B. – sequence: 10 givenname: Nicholas W. surname: Wood fullname: Wood, Nicholas W. – sequence: 11 givenname: Alexis surname: Brice fullname: Brice, Alexis – sequence: 12 givenname: Peter surname: Heutink fullname: Heutink, Peter – sequence: 13 givenname: Nigel surname: Williams fullname: Williams, Nigel – sequence: 14 givenname: Huw R. surname: Morris fullname: Morris, Huw R. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22427796$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1186_s12711_014_0081_5 crossref_primary_10_1177_1877718X241304814 crossref_primary_10_1016_j_cellsig_2018_10_019 crossref_primary_10_1007_s00439_025_02747_9 crossref_primary_10_1016_j_csbj_2020_07_003 crossref_primary_10_1016_j_cnur_2013_08_006 crossref_primary_10_3168_jds_2012_6435 crossref_primary_10_1159_000346790 crossref_primary_10_3168_jds_2014_9014 crossref_primary_10_1371_journal_pone_0048375 crossref_primary_10_1111_ahg_12304 crossref_primary_10_1016_j_ajhg_2018_02_013 crossref_primary_10_1007_s00415_013_7003_2 crossref_primary_10_1038_ejhg_2013_155 crossref_primary_10_1038_srep14315 crossref_primary_10_1186_s12864_017_4312_3 |
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| Copyright | COPYRIGHT 2012 Public Library of Science 2012. This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. 2012 |
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| CorporateAuthor | International Parkinson's Disease Genomics Consortium Wellcome Trust Case Control Consortium |
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| DOI | 10.1371/journal.pone.0028787 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Feature-1 content type line 23 Conceived and designed the experiments: HRM NMW LLK JS-S CS. Performed the experiments: JS-S LLK. Analyzed the data: LLK JS-S. Contributed reagents/materials/analysis tools: CS. Wrote the paper: LLK JS-S HRM NMW. Contributed samples: TG JH ABS NWW AB PH NMW HRM WTCCC2. Critically reviewed manuscript: MAN MM PAH JH AB NMW HRM JS-S LLK. a Membership of the International Parkinson's Disease Genomics Consortium is provided in the Acknowledgments. b Membership of the Wellcome Trust Case Control Consortium is provided in supporting information. |
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| SubjectTerms | Adult Age Aged Aged, 80 and over Alzheimer's disease Alzheimers disease Analysis Biology Bipolar disorder Brain research Cases (containers) Chromosome 19 Chromosomes, Human, Pair 19 - genetics Colorectal cancer Consortia Europe Gene sequencing Genes Genes, Recessive Genetic aspects Genetic diversity Genetic factors Genetic Predisposition to Disease - genetics Genetic variance Genetics Genome, Human - genetics Genome-Wide Association Study Genomes Genomics Genotyping Globalization Homozygosity Homozygote Humans Inbreeding Laboratories Loci Logistic Models Medical research Medicine Middle Aged Movement disorders Mutation Neurodegenerative diseases Neurology Neurosciences PARK7 protein Parkinson Disease - genetics Parkinson's disease Parkinsons disease Polymorphism, Single Nucleotide - genetics Population Predictive control PTEN-induced putative kinase Regression analysis Schizophrenia Sequence Analysis, DNA Single-nucleotide polymorphism United States |
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| Title | Cooperative Genome-Wide Analysis Shows Increased Homozygosity in Early Onset Parkinson's Disease |
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