Admixture mapping implicates 13q33.3 as ancestry-of-origin locus for Alzheimer disease in Hispanic and Latino populations
Alzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic (CH) populations. Such admixed populations, descended from more than one ancestral population, can present challenges for genetic studies, including li...
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| Veröffentlicht in: | HGG advances Jg. 4; H. 3; S. 100207 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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United States
Elsevier Inc
13.07.2023
Elsevier |
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| ISSN: | 2666-2477, 2666-2477 |
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| Abstract | Alzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic (CH) populations. Such admixed populations, descended from more than one ancestral population, can present challenges for genetic studies, including limited sample sizes and unique analytical constraints. Therefore, CH populations and other admixed populations have not been well represented in studies of AD, and much of the genetic variation contributing to AD risk in these populations remains unknown. Here, we conduct genome-wide analysis of AD in multiplex CH families from the Alzheimer Disease Sequencing Project (ADSP). We developed, validated, and applied an implementation of a logistic mixed model for admixture mapping with binary traits that leverages genetic ancestry to identify ancestry-of-origin loci contributing to AD. We identified three loci on chromosome 13q33.3 associated with reduced risk of AD, where associations were driven by Native American (NAM) ancestry. This AD admixture mapping signal spans the FAM155A, ABHD13, TNFSF13B, LIG4, and MYO16 genes and was supported by evidence for association in an independent sample from the Alzheimer’s Genetics in Argentina—Alzheimer Argentina consortium (AGA-ALZAR) study with considerable NAM ancestry. We also provide evidence of NAM haplotypes and key variants within 13q33.3 that segregate with AD in the ADSP whole-genome sequencing data. Interestingly, the widely used genome-wide association study approach failed to identify associations in this region. Our findings underscore the potential of leveraging genetic ancestry diversity in recently admixed populations to improve genetic mapping, in this case for AD-relevant loci.
We develop and implement a model for binary traits and related individuals that leverages diversity in genetic ancestry for admixture mapping. We apply the model to Hispanic Alzheimer disease samples to identify a region on chromosome 13q33.3 that contains protective sequence variants on haplotypes with ancestral native American ancestry. |
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| AbstractList | Alzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic (CH) populations. Such admixed populations, descended from more than one ancestral population, can present challenges for genetic studies, including limited sample sizes and unique analytical constraints. Therefore, CH populations and other admixed populations have not been well represented in studies of AD, and much of the genetic variation contributing to AD risk in these populations remains unknown. Here, we conduct genome-wide analysis of AD in multiplex CH families from the Alzheimer Disease Sequencing Project (ADSP). We developed, validated, and applied an implementation of a logistic mixed model for admixture mapping with binary traits that leverages genetic ancestry to identify ancestry-of-origin loci contributing to AD. We identified three loci on chromosome 13q33.3 associated with reduced risk of AD, where associations were driven by Native American (NAM) ancestry. This AD admixture mapping signal spans the FAM155A, ABHD13, TNFSF13B, LIG4, and MYO16 genes and was supported by evidence for association in an independent sample from the Alzheimer’s Genetics in Argentina—Alzheimer Argentina consortium (AGA-ALZAR) study with considerable NAM ancestry. We also provide evidence of NAM haplotypes and key variants within 13q33.3 that segregate with AD in the ADSP whole-genome sequencing data. Interestingly, the widely used genome-wide association study approach failed to identify associations in this region. Our findings underscore the potential of leveraging genetic ancestry diversity in recently admixed populations to improve genetic mapping, in this case for AD-relevant loci. We develop and implement a model for binary traits and related individuals that leverages diversity in genetic ancestry for admixture mapping. We apply the model to Hispanic Alzheimer disease samples to identify a region on chromosome 13q33.3 that contains protective sequence variants on haplotypes with ancestral native American ancestry. Alzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic (CH) populations. Such admixed populations, descended from more than one ancestral population, can present challenges for genetic studies, including limited sample sizes and unique analytical constraints. Therefore, CH populations and other admixed populations have not been well represented in studies of AD, and much of the genetic variation contributing to AD risk in these populations remains unknown. Here, we conduct genome-wide analysis of AD in multiplex CH families from the Alzheimer Disease Sequencing Project (ADSP). We developed, validated, and applied an implementation of a logistic mixed model for admixture mapping with binary traits that leverages genetic ancestry to identify ancestry-of-origin loci contributing to AD. We identified three loci on chromosome 13q33.3 associated with reduced risk of AD, where associations were driven by Native American (NAM) ancestry. This AD admixture mapping signal spans the FAM155A, ABHD13, TNFSF13B, LIG4, and MYO16 genes and was supported by evidence for association in an independent sample from the Alzheimer’s Genetics in Argentina—Alzheimer Argentina consortium (AGA-ALZAR) study with considerable NAM ancestry. We also provide evidence of NAM haplotypes and key variants within 13q33.3 that segregate with AD in the ADSP whole-genome sequencing data. Interestingly, the widely used genome-wide association study approach failed to identify associations in this region. Our findings underscore the potential of leveraging genetic ancestry diversity in recently admixed populations to improve genetic mapping, in this case for AD-relevant loci. We develop and implement a model for binary traits and related individuals that leverages diversity in genetic ancestry for admixture mapping. We apply the model to Hispanic Alzheimer disease samples to identify a region on chromosome 13q33.3 that contains protective sequence variants on haplotypes with ancestral native American ancestry. Alzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic (CH) populations. Such admixed populations, descended from more than one ancestral population, can present challenges for genetic studies, including limited sample sizes and unique analytical constraints. Therefore, CH populations and other admixed populations have not been well represented in studies of AD, and much of the genetic variation contributing to AD risk in these populations remains unknown. Here, we conduct genome-wide analysis of AD in multiplex CH families from the Alzheimer Disease Sequencing Project (ADSP). We developed, validated, and applied an implementation of a logistic mixed model for admixture mapping with binary traits that leverages genetic ancestry to identify ancestry-of-origin loci contributing to AD. We identified three loci on chromosome 13q33.3 associated with reduced risk of AD, where associations were driven by Native American (NAM) ancestry. This AD admixture mapping signal spans the FAM155A, ABHD13, TNFSF13B, LIG4, and MYO16 genes and was supported by evidence for association in an independent sample from the Alzheimer's Genetics in Argentina-Alzheimer Argentina consortium (AGA-ALZAR) study with considerable NAM ancestry. We also provide evidence of NAM haplotypes and key variants within 13q33.3 that segregate with AD in the ADSP whole-genome sequencing data. Interestingly, the widely used genome-wide association study approach failed to identify associations in this region. Our findings underscore the potential of leveraging genetic ancestry diversity in recently admixed populations to improve genetic mapping, in this case for AD-relevant loci.Alzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic (CH) populations. Such admixed populations, descended from more than one ancestral population, can present challenges for genetic studies, including limited sample sizes and unique analytical constraints. Therefore, CH populations and other admixed populations have not been well represented in studies of AD, and much of the genetic variation contributing to AD risk in these populations remains unknown. Here, we conduct genome-wide analysis of AD in multiplex CH families from the Alzheimer Disease Sequencing Project (ADSP). We developed, validated, and applied an implementation of a logistic mixed model for admixture mapping with binary traits that leverages genetic ancestry to identify ancestry-of-origin loci contributing to AD. We identified three loci on chromosome 13q33.3 associated with reduced risk of AD, where associations were driven by Native American (NAM) ancestry. This AD admixture mapping signal spans the FAM155A, ABHD13, TNFSF13B, LIG4, and MYO16 genes and was supported by evidence for association in an independent sample from the Alzheimer's Genetics in Argentina-Alzheimer Argentina consortium (AGA-ALZAR) study with considerable NAM ancestry. We also provide evidence of NAM haplotypes and key variants within 13q33.3 that segregate with AD in the ADSP whole-genome sequencing data. Interestingly, the widely used genome-wide association study approach failed to identify associations in this region. Our findings underscore the potential of leveraging genetic ancestry diversity in recently admixed populations to improve genetic mapping, in this case for AD-relevant loci. Alzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic (CH) populations. Such admixed populations, descended from more than one ancestral population, can present challenges for genetic studies, including limited sample sizes and unique analytical constraints. Therefore, CH populations and other admixed populations have not been well represented in studies of AD, and much of the genetic variation contributing to AD risk in these populations remains unknown. Here, we conduct genome-wide analysis of AD in multiplex CH families from the Alzheimer Disease Sequencing Project (ADSP). We developed, validated, and applied an implementation of a logistic mixed model for admixture mapping with binary traits that leverages genetic ancestry to identify ancestry-of-origin loci contributing to AD. We identified three loci on chromosome 13q33.3 associated with reduced risk of AD, where associations were driven by Native American (NAM) ancestry. This AD admixture mapping signal spans the FAM155A, ABHD13, TNFSF13B, LIG4, and MYO16 genes and was supported by evidence for association in an independent sample from the Alzheimer’s Genetics in Argentina—Alzheimer Argentina consortium (AGA-ALZAR) study with considerable NAM ancestry. We also provide evidence of NAM haplotypes and key variants within 13q33.3 that segregate with AD in the ADSP whole-genome sequencing data. Interestingly, the widely used genome-wide association study approach failed to identify associations in this region. Our findings underscore the potential of leveraging genetic ancestry diversity in recently admixed populations to improve genetic mapping, in this case for AD-relevant loci. Alzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic (CH) populations. Such admixed populations, descended from more than one ancestral population, can present challenges for genetic studies, including limited sample sizes and unique analytical constraints. Therefore, CH populations and other admixed populations have not been well represented in studies of AD, and much of the genetic variation contributing to AD risk in these populations remains unknown. Here, we conduct genome-wide analysis of AD in multiplex CH families from the Alzheimer Disease Sequencing Project (ADSP). We developed, validated, and applied an implementation of a logistic mixed model for admixture mapping with binary traits that leverages genetic ancestry to identify ancestry-of-origin loci contributing to AD. We identified three loci on chromosome 13q33.3 associated with reduced risk of AD, where associations were driven by Native American (NAM) ancestry. This AD admixture mapping signal spans the , , , and genes and was supported by evidence for association in an independent sample from the Alzheimer's Genetics in Argentina-Alzheimer Argentina consortium (AGA-ALZAR) study with considerable NAM ancestry. We also provide evidence of NAM haplotypes and key variants within 13q33.3 that segregate with AD in the ADSP whole-genome sequencing data. Interestingly, the widely used genome-wide association study approach failed to identify associations in this region. Our findings underscore the potential of leveraging genetic ancestry diversity in recently admixed populations to improve genetic mapping, in this case for AD-relevant loci. SummaryAlzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic (CH) populations. Such admixed populations, descended from more than one ancestral population, can present challenges for genetic studies, including limited sample sizes and unique analytical constraints. Therefore, CH populations and other admixed populations have not been well represented in studies of AD, and much of the genetic variation contributing to AD risk in these populations remains unknown. Here, we conduct genome-wide analysis of AD in multiplex CH families from the Alzheimer Disease Sequencing Project (ADSP). We developed, validated, and applied an implementation of a logistic mixed model for admixture mapping with binary traits that leverages genetic ancestry to identify ancestry-of-origin loci contributing to AD. We identified three loci on chromosome 13q33.3 associated with reduced risk of AD, where associations were driven by Native American (NAM) ancestry. This AD admixture mapping signal spans the FAM155A, ABHD13, TNFSF13B, LIG4, and MYO16 genes and was supported by evidence for association in an independent sample from the Alzheimer’s Genetics in Argentina—Alzheimer Argentina consortium (AGA-ALZAR) study with considerable NAM ancestry. We also provide evidence of NAM haplotypes and key variants within 13q33.3 that segregate with AD in the ADSP whole-genome sequencing data. Interestingly, the widely used genome-wide association study approach failed to identify associations in this region. Our findings underscore the potential of leveraging genetic ancestry diversity in recently admixed populations to improve genetic mapping, in this case for AD-relevant loci. |
| ArticleNumber | 100207 |
| Author | Dalmasso, Maria Carolina Nafikov, Rafael A. Sohi, Harkirat K. Boyken, Lisa A. Thornton, Timothy A. Bis, Joshua C. Satizabal, Claudia Grinde, Kelsey E. Temple, Seth Seshadri, Sudha Blue, Elizabeth E. Browning, Sharon R. Horimoto, Andrea R.V.R. Wijsman, Ellen M. Ramirez, Alfredo Nato, Alejandro Q. Brusco, Luis I. Morelli, Laura |
| Author_xml | – sequence: 1 givenname: Andrea R.V.R. surname: Horimoto fullname: Horimoto, Andrea R.V.R. email: andrearh@uw.edu organization: Department of Biostatistics, University of Washington, Seattle, WA 98195, USA – sequence: 2 givenname: Lisa A. surname: Boyken fullname: Boyken, Lisa A. organization: Department of Biostatistics, University of Washington, Seattle, WA 98195, USA – sequence: 3 givenname: Elizabeth E. surname: Blue fullname: Blue, Elizabeth E. organization: Division of Medical Genetics/Department of Medicine, University of Washington, Seattle, WA 98195, USA – sequence: 4 givenname: Kelsey E. surname: Grinde fullname: Grinde, Kelsey E. organization: Department of Biostatistics, University of Washington, Seattle, WA 98195, USA – sequence: 5 givenname: Rafael A. surname: Nafikov fullname: Nafikov, Rafael A. organization: Department of Biostatistics, University of Washington, Seattle, WA 98195, USA – sequence: 6 givenname: Harkirat K. surname: Sohi fullname: Sohi, Harkirat K. organization: Division of Medical Genetics/Department of Medicine, University of Washington, Seattle, WA 98195, USA – sequence: 7 givenname: Alejandro Q. surname: Nato fullname: Nato, Alejandro Q. organization: Division of Medical Genetics/Department of Medicine, University of Washington, Seattle, WA 98195, USA – sequence: 8 givenname: Joshua C. surname: Bis fullname: Bis, Joshua C. organization: Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, WA 98101, USA – sequence: 9 givenname: Luis I. surname: Brusco fullname: Brusco, Luis I. organization: CENECON - Center of Behavioural Neurology and Neuropsychiatry, School of Medicine, University of Buenos Aires, C1121A6B Buenos Aires, Argentina – sequence: 10 givenname: Laura surname: Morelli fullname: Morelli, Laura organization: Laboratory of Brain Aging and Neurodegeneration-Fundación Instituto Leloir-IIBBA- National Scientific and Technical Research Council (CONICET), C1405BWE Ciudad Autónoma de Buenos Aires, Argentina – sequence: 11 givenname: Alfredo surname: Ramirez fullname: Ramirez, Alfredo organization: Division of Neurogenetics and Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University of Cologne, Medical Faculty, 50937 Cologne, Germany – sequence: 12 givenname: Maria Carolina surname: Dalmasso fullname: Dalmasso, Maria Carolina organization: Division of Neurogenetics and Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University of Cologne, Medical Faculty, 50937 Cologne, Germany – sequence: 13 givenname: Seth surname: Temple fullname: Temple, Seth organization: Department of Statistics, University of Washington, Seattle, WA 98195, USA – sequence: 14 givenname: Claudia surname: Satizabal fullname: Satizabal, Claudia organization: Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases, UT Health San Antonio, San Antonio, TX 78229, USA – sequence: 15 givenname: Sharon R. surname: Browning fullname: Browning, Sharon R. organization: Department of Biostatistics, University of Washington, Seattle, WA 98195, USA – sequence: 16 givenname: Sudha surname: Seshadri fullname: Seshadri, Sudha organization: Department of Neurology, University of Texas, San Antonio, TX 78229, USA – sequence: 17 givenname: Ellen M. surname: Wijsman fullname: Wijsman, Ellen M. email: wijsman@uw.edu organization: Department of Biostatistics, University of Washington, Seattle, WA 98195, USA – sequence: 18 givenname: Timothy A. surname: Thornton fullname: Thornton, Timothy A. organization: Department of Biostatistics, University of Washington, Seattle, WA 98195, USA |
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| Keywords | haplotype population structure local ancestry non-coding gene mapping whole genome sequence protective multi-ethnic rare variation |
| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Present address: La Jolla Labs Inc., La Jolla, CA 92037, USA Present address: Zymeworks Biopharmaceuticals, Inc., Seattle, WA 98101, USA Present address: Division of Aging, Brigham and Women’s Hospital, Boston, MA, USA Lead contact |
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| Snippet | Alzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic (CH)... SummaryAlzheimer disease (AD) is the most common form of senile dementia, with high incidence late in life in many populations including Caribbean Hispanic... |
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| SubjectTerms | Alzheimer disease Alzheimer Disease - genetics ancestry Argentina Caribbean Ethnicity gene mapping Genetic Loci - genetics genetic variation Genetics Genome-Wide Association Study genomics haplotype haplotypes Hispanic or Latino - genetics human genetics Humans Latinos local ancestry loci multi-ethnic non-coding population structure protective rare variation risk risk reduction statistical models whole genome sequence |
| Title | Admixture mapping implicates 13q33.3 as ancestry-of-origin locus for Alzheimer disease in Hispanic and Latino populations |
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