Genome scan of age-at-onset in the NIMH Alzheimer disease sample uncovers multiple loci, along with evidence of both genetic and sample heterogeneity

Alzheimer's disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in rare early onset AD, only the APOE gene is known to have a high contribution to risk of the common late‐onset form of the disease (LOAD,...

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Published inAmerican journal of medical genetics. Part B, Neuropsychiatric genetics Vol. 156B; no. 7; pp. 785 - 798
Main Authors Choi, Yoonha, Marchani, Elizabeth E., Bird, Thomas D., Steinbart, Ellen J., Blacker, Deborah, Wijsman, Ellen M.
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.12.2011
Wiley-Liss
Subjects
Adult
Adult and adolescent clinical studies
Age
Age of Onset
Aged
Aged, 80 and over
Alzheimer Disease - epidemiology
Alzheimer Disease - genetics
Alzheimer's disease
Apolipoprotein E
Bayes Theorem
Bayesian
Biological and medical sciences
Chromosome 1
chromosome 10
chromosome 19
chromosome 7
Chromosome Mapping
Chromosome Segregation - genetics
Chromosomes, Human - genetics
Classical genetics, quantitative genetics, hybrids
Data processing
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
dementia
Fundamental and applied biological sciences. Psychology
Genetic Heterogeneity
Genetics of eukaryotes. Biological and molecular evolution
Genome-Wide Association Study
Genomes
genomics
Genotypes
Human
Humans
linkage analysis
Lod Score
MCMC
Medical genetics
Medical sciences
Middle Aged
Models, Genetic
Monte Carlo Method
National Institute of Mental Health (U.S.)
Neurodegenerative diseases
Neurology
oligogenic
Organic mental disorders. Neuropsychology
Pedigree
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Quantitative Trait Loci - genetics
Reproducibility of Results
Risk factors
United States - epidemiology
United States
Genetic mapping
Nervous system diseases
Multiple
Alzheimer disease
Pathogenesis
Sample
Bayesian
MCMC
Genetic determinism
Cerebral disorder
oligogenic
Heterogeneity
Age of onset
linkage analysis
Central nervous system disease
Genetic linkage
Genetics
dementia
Degenerative disease
Genome
Locus
Online AccessGet full text
ISSN1552-4841
1552-485X
1552-485X
DOI10.1002/ajmg.b.31220

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Abstract Alzheimer's disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in rare early onset AD, only the APOE gene is known to have a high contribution to risk of the common late‐onset form of the disease (LOAD, onset >60 years). APOE genotypes vary in their AD risk as well as age‐at‐onset distributions, and it is likely that other loci will similarly affect AD age‐at‐onset. Here we present the first analysis of age‐at‐onset in the NIMH LOAD sample that allows for both a multilocus trait model and genetic heterogeneity among the contributing sites, while at the same time accommodating age censoring, effects of known genetic covariates, and full pedigree and marker information. The results provide evidence for genomic regions not previously implicated in this data set, including regions on chromosomes 7q, 15, and 19p. They also affirm evidence for loci on chromosomes 1q, 6p, 9q, 11, and, of course, the APOE locus on 19q, all of which have been reported previously in the same sample. The analyses failed to find evidence for linkage to chromosome 10 with inclusion of unaffected subjects and extended pedigrees. Several regions implicated in these analyses in the NIMH sample have been previously reported in genome scans of other AD samples. These results, therefore, provide independent confirmation of AD loci in family‐based samples on chromosomes 1q, 7q, 19p, and suggest that further efforts towards identifying the underlying causal loci are warranted. © 2011 Wiley‐Liss, Inc.
AbstractList Alzheimer's disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in rare early onset AD, only the APOE gene is known to have a high contribution to risk of the common late-onset form of the disease (LOAD, onset >60 years). APOE genotypes vary in their AD risk as well as age-at-onset distributions, and it is likely that other loci will similarly affect AD age-at-onset. Here we present the first analysis of age-at-onset in the NIMH LOAD sample that allows for both a multilocus trait model and genetic heterogeneity among the contributing sites, while at the same time accommodating age censoring, effects of known genetic covariates, and full pedigree and marker information. The results provide evidence for genomic regions not previously implicated in this data set, including regions on chromosomes 7q, 15, and 19p. They also affirm evidence for loci on chromosomes 1q, 6p, 9q, 11, and, of course, the APOE locus on 19q, all of which have been reported previously in the same sample. The analyses failed to find evidence for linkage to chromosome 10 with inclusion of unaffected subjects and extended pedigrees. Several regions implicated in these analyses in the NIMH sample have been previously reported in genome scans of other AD samples. These results, therefore, provide independent confirmation of AD loci in family-based samples on chromosomes 1q, 7q, 19p, and suggest that further efforts towards identifying the underlying causal loci are warranted.
Alzheimer's disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in rare early onset AD, only the APOE gene is known to have a high contribution to risk of the common late‐onset form of the disease (LOAD, onset >60 years). APOE genotypes vary in their AD risk as well as age‐at‐onset distributions, and it is likely that other loci will similarly affect AD age‐at‐onset. Here we present the first analysis of age‐at‐onset in the NIMH LOAD sample that allows for both a multilocus trait model and genetic heterogeneity among the contributing sites, while at the same time accommodating age censoring, effects of known genetic covariates, and full pedigree and marker information. The results provide evidence for genomic regions not previously implicated in this data set, including regions on chromosomes 7q, 15, and 19p. They also affirm evidence for loci on chromosomes 1q, 6p, 9q, 11, and, of course, the APOE locus on 19q, all of which have been reported previously in the same sample. The analyses failed to find evidence for linkage to chromosome 10 with inclusion of unaffected subjects and extended pedigrees. Several regions implicated in these analyses in the NIMH sample have been previously reported in genome scans of other AD samples. These results, therefore, provide independent confirmation of AD loci in family‐based samples on chromosomes 1q, 7q, 19p, and suggest that further efforts towards identifying the underlying causal loci are warranted. © 2011 Wiley‐Liss, Inc.
Alzheimer's disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in rare early onset AD, only the APOE gene is known to have a high contribution to risk of the common late‐onset form of the disease (LOAD, onset >60 years). APOE genotypes vary in their AD risk as well as age‐at‐onset distributions, and it is likely that other loci will similarly affect AD age‐at‐onset. Here we present the first analysis of age‐at‐onset in the NIMH LOAD sample that allows for both a multilocus trait model and genetic heterogeneity among the contributing sites, while at the same time accommodating age censoring, effects of known genetic covariates, and full pedigree and marker information. The results provide evidence for genomic regions not previously implicated in this data set, including regions on chromosomes 7q, 15, and 19p. They also affirm evidence for loci on chromosomes 1q, 6p, 9q, 11, and, of course, the APOE locus on 19q, all of which have been reported previously in the same sample. The analyses failed to find evidence for linkage to chromosome 10 with inclusion of unaffected subjects and extended pedigrees. Several regions implicated in these analyses in the NIMH sample have been previously reported in genome scans of other AD samples. These results, therefore, provide independent confirmation of AD loci in family‐based samples on chromosomes 1q, 7q, 19p, and suggest that further efforts towards identifying the underlying causal loci are warranted. © 2011 Wiley‐Liss, Inc.
Alzheimer’s disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in rare early-onset AD, only the APOE gene is known to have a high contribution to risk of the common late-onset form of the disease (LOAD, onset > 60 years). APOE genotypes vary in their AD risk as well as age-at-onset distributions, and it is likely that other loci will similarly affect AD age-at-onset. Here we present the first analysis of age-at-onset in the NIMH LOAD sample that allows for both a multilocus trait model and genetic heterogeneity among the contributing sites, while at the same time accommodating age censoring, effects of known genetic covariates, and full pedigree and marker information. The results provide evidence for genomic regions not previously implicated in this data set, including regions on chromosomes 7q, 15, and 19p. They also affirm evidence for loci on chromosomes 1q, 6p, 9q, 11, and, of course, the APOE locus on 19q, all of which have been reported previously in the same sample. The analyses failed to find evidence for linkage to chromosome 10 with inclusion of unaffected subjects and extended pedigrees. Several regions implicated in these analyses in the NIMH sample have been previously reported in genome scans of other AD samples. These results, therefore, provide independent confirmation of AD loci in family-based samples on chromosomes 1q, 7q, 19p, and suggest that further efforts towards identifying the underlying causal loci are warranted.
Alzheimer's disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in rare early onset AD, only the APOE gene is known to have a high contribution to risk of the common late-onset form of the disease (LOAD, onset >60 years). APOE genotypes vary in their AD risk as well as age-at-onset distributions, and it is likely that other loci will similarly affect AD age-at-onset. Here we present the first analysis of age-at-onset in the NIMH LOAD sample that allows for both a multilocus trait model and genetic heterogeneity among the contributing sites, while at the same time accommodating age censoring, effects of known genetic covariates, and full pedigree and marker information. The results provide evidence for genomic regions not previously implicated in this data set, including regions on chromosomes 7q, 15, and 19p. They also affirm evidence for loci on chromosomes 1q, 6p, 9q, 11, and, of course, the APOE locus on 19q, all of which have been reported previously in the same sample. The analyses failed to find evidence for linkage to chromosome 10 with inclusion of unaffected subjects and extended pedigrees. Several regions implicated in these analyses in the NIMH sample have been previously reported in genome scans of other AD samples. These results, therefore, provide independent confirmation of AD loci in family-based samples on chromosomes 1q, 7q, 19p, and suggest that further efforts towards identifying the underlying causal loci are warranted.Alzheimer's disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in rare early onset AD, only the APOE gene is known to have a high contribution to risk of the common late-onset form of the disease (LOAD, onset >60 years). APOE genotypes vary in their AD risk as well as age-at-onset distributions, and it is likely that other loci will similarly affect AD age-at-onset. Here we present the first analysis of age-at-onset in the NIMH LOAD sample that allows for both a multilocus trait model and genetic heterogeneity among the contributing sites, while at the same time accommodating age censoring, effects of known genetic covariates, and full pedigree and marker information. The results provide evidence for genomic regions not previously implicated in this data set, including regions on chromosomes 7q, 15, and 19p. They also affirm evidence for loci on chromosomes 1q, 6p, 9q, 11, and, of course, the APOE locus on 19q, all of which have been reported previously in the same sample. The analyses failed to find evidence for linkage to chromosome 10 with inclusion of unaffected subjects and extended pedigrees. Several regions implicated in these analyses in the NIMH sample have been previously reported in genome scans of other AD samples. These results, therefore, provide independent confirmation of AD loci in family-based samples on chromosomes 1q, 7q, 19p, and suggest that further efforts towards identifying the underlying causal loci are warranted.
Alzheimer's disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in rare early onset AD, only the APOE gene is known to have a high contribution to risk of the common late-onset form of the disease (LOAD, onset >60 years). APOE genotypes vary in their AD risk as well as age-at-onset distributions, and it is likely that other loci will similarly affect AD age-at-onset. Here we present the first analysis of age-at-onset in the NIMH LOAD sample that allows for both a multilocus trait model and genetic heterogeneity among the contributing sites, while at the same time accommodating age censoring, effects of known genetic covariates, and full pedigree and marker information. The results provide evidence for genomic regions not previously implicated in this data set, including regions on chromosomes 7q, 15, and 19p. They also affirm evidence for loci on chromosomes 1q, 6p, 9q, 11, and, of course, the APOE locus on 19q, all of which have been reported previously in the same sample. The analyses failed to find evidence for linkage to chromosome 10 with inclusion of unaffected subjects and extended pedigrees. Several regions implicated in these analyses in the NIMH sample have been previously reported in genome scans of other AD samples. These results, therefore, provide independent confirmation of AD loci in family-based samples on chromosomes 1q, 7q, 19p, and suggest that further efforts towards identifying the underlying causal loci are warranted. copyright 2011 Wiley-Liss, Inc.
Author Bird, Thomas D.
Blacker, Deborah
Wijsman, Ellen M.
Choi, Yoonha
Steinbart, Ellen J.
Marchani, Elizabeth E.
AuthorAffiliation 4 Department of Neurology, University of Washington, Seattle, WA
3 Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle Division, Seattle, WA
1 Department of Biostatistics, University of Washington, Seattle, WA
6 Department of Genome Sciences, University of Washington, Seattle, WA
5 Department of Psychiatry, Massachusetts General Hospital/Harvard Medical School; Dept of Epidemiology, Harvard School of Public Health; Boston, MA
2 Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA
AuthorAffiliation_xml – name: 4 Department of Neurology, University of Washington, Seattle, WA
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CitedBy_id crossref_primary_10_1002_ajmg_b_32133
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IsPeerReviewed true
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Issue 7
Keywords Genetic mapping
Nervous system diseases
Multiple
Alzheimer disease
Pathogenesis
Sample
Bayesian
MCMC
Genetic determinism
Cerebral disorder
oligogenic
Heterogeneity
Age of onset
linkage analysis
Central nervous system disease
Genetic linkage
Genetics
dementia
Degenerative disease
Genome
Locus
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
CC BY 4.0
Copyright © 2011 Wiley-Liss, Inc.
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Notes National Institute of Mental Health (NIMH) Alzheimer Disease Genetics Initiative - No. U01 MH46281; No. U01 MH46290; No. U01 MH46373
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National Institute of Health (NIH) - No. P50 AG005136; No. T32 AG000258
ArticleID:AJMG31220
How to Cite this Article: Choi Y, Marchani EE, Bird TD, Steinbart EJ, Blacker D, Wijsman EM. 2011. Genome Scan of Age-at-Onset in the NIMH Alzheimer Disease Sample Uncovers Multiple Loci, Along With Evidence of Both Genetic and Sample Heterogeneity. Am J Med Genet Part B 156:785-798.
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How to Cite this Article: Choi Y, Marchani EE, Bird TD, Steinbart EJ, Blacker D, Wijsman EM. 2011. Genome Scan of Age‐at‐Onset in the NIMH Alzheimer Disease Sample Uncovers Multiple Loci, Along With Evidence of Both Genetic and Sample Heterogeneity. Am J Med Genet Part B 156:785–798.
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PublicationDate December 2011
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  text: December 2011
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PublicationTitle American journal of medical genetics. Part B, Neuropsychiatric genetics
PublicationTitleAlternate Am. J. Med. Genet
PublicationYear 2011
Publisher Wiley Subscription Services, Inc., A Wiley Company
Wiley-Liss
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2007; 39
2005; 135B
2009; 41
2009; 84
2009; 81
2010; 303
2004; 28
1997; 48
2010; 153B
2002; 114
2008; 9
2008; 147B
2008; 32
1998; 81
1995; 375
2008; 1
2000; 290
2003; 12
1987; 44
2004; 75
2006; 63
2006; 61
1997; 52
1989; 262
2005; 132B
1999; 15
1991; 349
2001; 57
1998; 12
2007; 68
2005; 77
1998; 55
2010; 34
1995; 50
2009; 62
1997; 61
1995; 90
2002; 30
2005; 352
2010; 127
2000; 66
1994; 150
2008; 16
2006; 15
1993; 261
1999; 64
1999; 63
1999; 8
1969; 19
2003; 73
2011; 7
2001; 65
2007; 16
2006; 141B
2009; 30
1995; 82
1986; 20
2000; 35
1995; 45
1984; 34
1995; 269
2007; 81
1996; 273
1996; 46
2003; 100
1994; 7
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Snippet Alzheimer's disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in...
Alzheimer’s disease (AD) is a common neurodegenerative disorder of late life with a complex genetic basis. Although several genes are known to play a role in...
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pubmed
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Enrichment Source
Publisher
StartPage 785
SubjectTerms Adult
Adult and adolescent clinical studies
Age
Age of Onset
Aged
Aged, 80 and over
Alzheimer Disease - epidemiology
Alzheimer Disease - genetics
Alzheimer's disease
Apolipoprotein E
Bayes Theorem
Bayesian
Biological and medical sciences
Chromosome 1
chromosome 10
chromosome 19
chromosome 7
Chromosome Mapping
Chromosome Segregation - genetics
Chromosomes, Human - genetics
Classical genetics, quantitative genetics, hybrids
Data processing
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
dementia
Fundamental and applied biological sciences. Psychology
Genetic Heterogeneity
Genetics of eukaryotes. Biological and molecular evolution
Genome-Wide Association Study
Genomes
genomics
Genotypes
Human
Humans
linkage analysis
Lod Score
MCMC
Medical genetics
Medical sciences
Middle Aged
Models, Genetic
Monte Carlo Method
National Institute of Mental Health (U.S.)
Neurodegenerative diseases
Neurology
oligogenic
Organic mental disorders. Neuropsychology
Pedigree
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Quantitative Trait Loci - genetics
Reproducibility of Results
Risk factors
United States - epidemiology
Title Genome scan of age-at-onset in the NIMH Alzheimer disease sample uncovers multiple loci, along with evidence of both genetic and sample heterogeneity
URI https://api.istex.fr/ark:/67375/WNG-F52W072M-1/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fajmg.b.31220
https://www.ncbi.nlm.nih.gov/pubmed/21812099
https://www.proquest.com/docview/1017975666
https://www.proquest.com/docview/888092552
https://pubmed.ncbi.nlm.nih.gov/PMC3168696
Volume 156B
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