Genetic architecture of Alzheimer's disease

Advances in genetic and genomic technologies over the last thirty years have greatly enhanced our knowledge concerning the genetic architecture of Alzheimer's disease (AD). Several genes including APP, PSEN1, PSEN2, and APOE have been shown to exhibit large effects on disease susceptibility, wi...

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Published inNeurobiology of disease Vol. 143; p. 104976
Main Authors Neuner, Sarah M., TCW, Julia, Goate, Alison M.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.09.2020
Elsevier
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Abstract Advances in genetic and genomic technologies over the last thirty years have greatly enhanced our knowledge concerning the genetic architecture of Alzheimer's disease (AD). Several genes including APP, PSEN1, PSEN2, and APOE have been shown to exhibit large effects on disease susceptibility, with the remaining risk loci having much smaller effects on AD risk. Notably, common genetic variants impacting AD are not randomly distributed across the genome. Instead, these variants are enriched within regulatory elements active in human myeloid cells, and to a lesser extent liver cells, implicating these cell and tissue types as critical to disease etiology. Integrative approaches are emerging as highly effective for identifying the specific target genes through which AD risk variants act and will likely yield important insights related to potential therapeutic targets in the coming years. In the future, additional consideration of sex- and ethnicity-specific contributions to risk as well as the contribution of complex gene-gene and gene-environment interactions will likely be necessary to further improve our understanding of AD genetic architecture.
AbstractList Advances in genetic and genomic technologies over the last thirty years have greatly enhanced our knowledge concerning the genetic architecture of Alzheimer's disease (AD). Several genes including APP, PSEN1, PSEN2, and APOE have been shown to exhibit large effects on disease susceptibility, with the remaining risk loci having much smaller effects on AD risk. Notably, common genetic variants impacting AD are not randomly distributed across the genome. Instead, these variants are enriched within regulatory elements active in human myeloid cells, and to a lesser extent liver cells, implicating these cell and tissue types as critical to disease etiology. Integrative approaches are emerging as highly effective for identifying the specific target genes through which AD risk variants act and will likely yield important insights related to potential therapeutic targets in the coming years. In the future, additional consideration of sex- and ethnicity-specific contributions to risk as well as the contribution of complex gene-gene and gene-environment interactions will likely be necessary to further improve our understanding of AD genetic architecture.
Advances in genetic and genomic technologies over the last thirty years have greatly enhanced our knowledge concerning the genetic architecture of Alzheimer’s disease (AD). Several genes including APP , PSEN1 , PSEN2 , and APOE have been shown to exhibit large effects on disease susceptibility, with the remaining risk loci having much smaller effects on AD risk. Notably, common genetic variants impacting AD are not randomly distributed across the genome. Instead, these variants are enriched within regulatory elements active in human myeloid cells, and to a lesser extent liver cells, implicating these cell and tissue types as critical to disease etiology. Integrative approaches are emerging as highly effective for identifying the specific target genes through which AD risk variants act and will likely yield important insights related to potential therapeutic targets in the coming years. In the future, additional consideration of sex- and ethnicity-specific contributions to risk as well as the contribution of complex gene-gene and gene-environment interactions will likely be necessary to further improve our understanding of AD genetic architecture.
Advances in genetic and genomic technologies over the last thirty years have greatly enhanced our knowledge concerning the genetic architecture of Alzheimer's disease (AD). Several genes including APP, PSEN1, PSEN2, and APOE have been shown to exhibit large effects on disease susceptibility, with the remaining risk loci having much smaller effects on AD risk. Notably, common genetic variants impacting AD are not randomly distributed across the genome. Instead, these variants are enriched within regulatory elements active in human myeloid cells, and to a lesser extent liver cells, implicating these cell and tissue types as critical to disease etiology. Integrative approaches are emerging as highly effective for identifying the specific target genes through which AD risk variants act and will likely yield important insights related to potential therapeutic targets in the coming years. In the future, additional consideration of sex- and ethnicity-specific contributions to risk as well as the contribution of complex gene-gene and gene-environment interactions will likely be necessary to further improve our understanding of AD genetic architecture.Advances in genetic and genomic technologies over the last thirty years have greatly enhanced our knowledge concerning the genetic architecture of Alzheimer's disease (AD). Several genes including APP, PSEN1, PSEN2, and APOE have been shown to exhibit large effects on disease susceptibility, with the remaining risk loci having much smaller effects on AD risk. Notably, common genetic variants impacting AD are not randomly distributed across the genome. Instead, these variants are enriched within regulatory elements active in human myeloid cells, and to a lesser extent liver cells, implicating these cell and tissue types as critical to disease etiology. Integrative approaches are emerging as highly effective for identifying the specific target genes through which AD risk variants act and will likely yield important insights related to potential therapeutic targets in the coming years. In the future, additional consideration of sex- and ethnicity-specific contributions to risk as well as the contribution of complex gene-gene and gene-environment interactions will likely be necessary to further improve our understanding of AD genetic architecture.
ArticleNumber 104976
Author TCW, Julia
Neuner, Sarah M.
Goate, Alison M.
AuthorAffiliation b Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, U.S.A
a Nash Department of Neuroscience, Ronald M. Loeb Center for Alzheimer’s Disease, Icahn School of Medicine at Mount Sinai, New York, U.S.A
AuthorAffiliation_xml – name: b Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, U.S.A
– name: a Nash Department of Neuroscience, Ronald M. Loeb Center for Alzheimer’s Disease, Icahn School of Medicine at Mount Sinai, New York, U.S.A
Author_xml – sequence: 1
  givenname: Sarah M.
  surname: Neuner
  fullname: Neuner, Sarah M.
  organization: Nash Department of Neuroscience, Ronald M. Loeb Center for Alzheimer’s Disease, Icahn School of Medicine at Mount Sinai, New York, USA
– sequence: 2
  givenname: Julia
  orcidid: 0000-0002-3054-9374
  surname: TCW
  fullname: TCW, Julia
  organization: Nash Department of Neuroscience, Ronald M. Loeb Center for Alzheimer’s Disease, Icahn School of Medicine at Mount Sinai, New York, USA
– sequence: 3
  givenname: Alison M.
  orcidid: 0000-0002-0576-2472
  surname: Goate
  fullname: Goate, Alison M.
  email: alison.goate@mssm.edu
  organization: Nash Department of Neuroscience, Ronald M. Loeb Center for Alzheimer’s Disease, Icahn School of Medicine at Mount Sinai, New York, USA
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Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.
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content type line 23
Authors contributed equally
9. Author Contributions
SMN, JTCW, and AMG wrote the manuscript. SMN and JTCW generated the table and the figure. All authors discussed and reviewed the manuscript.
ORCID 0000-0002-0576-2472
0000-0002-3054-9374
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PublicationTitle Neurobiology of disease
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  issue: 10
  year: 2009
  ident: 10.1016/j.nbd.2020.104976_bb0745
  article-title: Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer’s disease
  publication-title: Nature genetics
  doi: 10.1038/ng.439
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Snippet Advances in genetic and genomic technologies over the last thirty years have greatly enhanced our knowledge concerning the genetic architecture of Alzheimer's...
Advances in genetic and genomic technologies over the last thirty years have greatly enhanced our knowledge concerning the genetic architecture of Alzheimer’s...
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Title Genetic architecture of Alzheimer's disease
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0969996120302515
https://dx.doi.org/10.1016/j.nbd.2020.104976
https://www.ncbi.nlm.nih.gov/pubmed/32565066
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Volume 143
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