Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes

Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer’s disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. Previously, we showed that AD risk alle...

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Published inNature communications Vol. 12; no. 1; pp. 1610 - 14
Main Authors Novikova, Gloriia, Kapoor, Manav, TCW, Julia, Abud, Edsel M., Efthymiou, Anastasia G., Chen, Steven X., Cheng, Haoxiang, Fullard, John F., Bendl, Jaroslav, Liu, Yiyuan, Roussos, Panos, Björkegren, Johan LM, Liu, Yunlong, Poon, Wayne W., Hao, Ke, Marcora, Edoardo, Goate, Alison M.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 12.03.2021
Nature Publishing Group
Nature Portfolio
Subjects
631/114/2785
631/208/191
631/378/1689/1283
631/378/371
Alleles
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer's disease
Annotations
Datasets
Enhancers
Gene expression
Gene Expression Regulation
Gene mapping
Gene regulation
Genes
Genetic Predisposition to Disease - genetics
Genetics
Genome-wide association studies
Genome-Wide Association Study
Genomics
Health risks
Humanities and Social Sciences
Humans
Induced Pluripotent Stem Cells - metabolism
Loci
Macrophages
Microglia
Microglia - metabolism
Monocytes
multidisciplinary
Myeloid Cells
Neurodegenerative diseases
Nominations
Pathogenesis
Pluripotency
Regulatory sequences
Regulatory Sequences, Nucleic Acid - genetics
Risk
Science
Science (multidisciplinary)
Stem cells
Transcriptome
Online AccessGet full text

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Abstract Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer’s disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. Previously, we showed that AD risk alleles are enriched in myeloid-specific epigenomic annotations. Here, we show that they are specifically enriched in active enhancers of monocytes, macrophages and microglia. We integrated AD GWAS with myeloid epigenomic and transcriptomic datasets using analytical approaches to link myeloid enhancer activity to target gene expression regulation and AD risk modification. We identify AD risk enhancers and nominate candidate causal genes among their likely targets (including AP4E1, AP4M1, APBB3, BIN1, MS4A4A, MS4A6A, PILRA, RABEP1, SPI1, TP53INP1 , and ZYX ) in twenty loci. Fine-mapping of these enhancers nominates candidate functional variants that likely modify AD risk by regulating gene expression in myeloid cells. In the MS4A locus we identified a single candidate functional variant and validated it in human induced pluripotent stem cell (hiPSC)-derived microglia and brain. Taken together, this study integrates AD GWAS with multiple myeloid genomic datasets to investigate the mechanisms of AD risk alleles and nominates candidate functional variants, regulatory elements and genes that likely modulate disease susceptibility. This study integrates Alzheimer’s disease (AD) GWAS data with myeloid cell genomics, and reports that myeloid active enhancers are most burdened by AD risk alleles. The authors also nominate candidate causal regulatory elements, variants and genes that likely modulate the risk for AD.
AbstractList Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer’s disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. Previously, we showed that AD risk alleles are enriched in myeloid-specific epigenomic annotations. Here, we show that they are specifically enriched in active enhancers of monocytes, macrophages and microglia. We integrated AD GWAS with myeloid epigenomic and transcriptomic datasets using analytical approaches to link myeloid enhancer activity to target gene expression regulation and AD risk modification. We identify AD risk enhancers and nominate candidate causal genes among their likely targets (including AP4E1, AP4M1, APBB3, BIN1, MS4A4A, MS4A6A, PILRA, RABEP1, SPI1, TP53INP1 , and ZYX ) in twenty loci. Fine-mapping of these enhancers nominates candidate functional variants that likely modify AD risk by regulating gene expression in myeloid cells. In the MS4A locus we identified a single candidate functional variant and validated it in human induced pluripotent stem cell (hiPSC)-derived microglia and brain. Taken together, this study integrates AD GWAS with multiple myeloid genomic datasets to investigate the mechanisms of AD risk alleles and nominates candidate functional variants, regulatory elements and genes that likely modulate disease susceptibility. This study integrates Alzheimer’s disease (AD) GWAS data with myeloid cell genomics, and reports that myeloid active enhancers are most burdened by AD risk alleles. The authors also nominate candidate causal regulatory elements, variants and genes that likely modulate the risk for AD.
Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer's disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. Previously, we showed that AD risk alleles are enriched in myeloid-specific epigenomic annotations. Here, we show that they are specifically enriched in active enhancers of monocytes, macrophages and microglia. We integrated AD GWAS with myeloid epigenomic and transcriptomic datasets using analytical approaches to link myeloid enhancer activity to target gene expression regulation and AD risk modification. We identify AD risk enhancers and nominate candidate causal genes among their likely targets (including AP4E1, AP4M1, APBB3, BIN1, MS4A4A, MS4A6A, PILRA, RABEP1, SPI1, TP53INP1, and ZYX) in twenty loci. Fine-mapping of these enhancers nominates candidate functional variants that likely modify AD risk by regulating gene expression in myeloid cells. In the MS4A locus we identified a single candidate functional variant and validated it in human induced pluripotent stem cell (hiPSC)-derived microglia and brain. Taken together, this study integrates AD GWAS with multiple myeloid genomic datasets to investigate the mechanisms of AD risk alleles and nominates candidate functional variants, regulatory elements and genes that likely modulate disease susceptibility.
Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer’s disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. Previously, we showed that AD risk alleles are enriched in myeloid-specific epigenomic annotations. Here, we show that they are specifically enriched in active enhancers of monocytes, macrophages and microglia. We integrated AD GWAS with myeloid epigenomic and transcriptomic datasets using analytical approaches to link myeloid enhancer activity to target gene expression regulation and AD risk modification. We identify AD risk enhancers and nominate candidate causal genes among their likely targets (including AP4E1, AP4M1, APBB3, BIN1, MS4A4A, MS4A6A, PILRA, RABEP1, SPI1, TP53INP1 , and ZYX ) in twenty loci. Fine-mapping of these enhancers nominates candidate functional variants that likely modify AD risk by regulating gene expression in myeloid cells. In the MS4A locus we identified a single candidate functional variant and validated it in human induced pluripotent stem cell (hiPSC)-derived microglia and brain. Taken together, this study integrates AD GWAS with multiple myeloid genomic datasets to investigate the mechanisms of AD risk alleles and nominates candidate functional variants, regulatory elements and genes that likely modulate disease susceptibility.
This study integrates Alzheimer’s disease (AD) GWAS data with myeloid cell genomics, and reports that myeloid active enhancers are most burdened by AD risk alleles. The authors also nominate candidate causal regulatory elements, variants and genes that likely modulate the risk for AD.
Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer's disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. Previously, we showed that AD risk alleles are enriched in myeloid-specific epigenomic annotations. Here, we show that they are specifically enriched in active enhancers of monocytes, macrophages and microglia. We integrated AD GWAS with myeloid epigenomic and transcriptomic datasets using analytical approaches to link myeloid enhancer activity to target gene expression regulation and AD risk modification. We identify AD risk enhancers and nominate candidate causal genes among their likely targets (including AP4E1, AP4M1, APBB3, BIN1, MS4A4A, MS4A6A, PILRA, RABEP1, SPI1, TP53INP1, and ZYX) in twenty loci. Fine-mapping of these enhancers nominates candidate functional variants that likely modify AD risk by regulating gene expression in myeloid cells. In the MS4A locus we identified a single candidate functional variant and validated it in human induced pluripotent stem cell (hiPSC)-derived microglia and brain. Taken together, this study integrates AD GWAS with multiple myeloid genomic datasets to investigate the mechanisms of AD risk alleles and nominates candidate functional variants, regulatory elements and genes that likely modulate disease susceptibility.Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer's disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. Previously, we showed that AD risk alleles are enriched in myeloid-specific epigenomic annotations. Here, we show that they are specifically enriched in active enhancers of monocytes, macrophages and microglia. We integrated AD GWAS with myeloid epigenomic and transcriptomic datasets using analytical approaches to link myeloid enhancer activity to target gene expression regulation and AD risk modification. We identify AD risk enhancers and nominate candidate causal genes among their likely targets (including AP4E1, AP4M1, APBB3, BIN1, MS4A4A, MS4A6A, PILRA, RABEP1, SPI1, TP53INP1, and ZYX) in twenty loci. Fine-mapping of these enhancers nominates candidate functional variants that likely modify AD risk by regulating gene expression in myeloid cells. In the MS4A locus we identified a single candidate functional variant and validated it in human induced pluripotent stem cell (hiPSC)-derived microglia and brain. Taken together, this study integrates AD GWAS with multiple myeloid genomic datasets to investigate the mechanisms of AD risk alleles and nominates candidate functional variants, regulatory elements and genes that likely modulate disease susceptibility.
Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer’s disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. Previously, we showed that AD risk alleles are enriched in myeloid-specific epigenomic annotations. Here, we show that they are specifically enriched in active enhancers of monocytes, macrophages and microglia. We integrated AD GWAS with myeloid epigenomic and transcriptomic datasets using analytical approaches to link myeloid enhancer activity to target gene expression regulation and AD risk modification. We identify AD risk enhancers and nominate candidate causal genes among their likely targets (including AP4E1, AP4M1, APBB3, BIN1, MS4A4A, MS4A6A, PILRA, RABEP1, SPI1, TP53INP1, and ZYX) in twenty loci. Fine-mapping of these enhancers nominates candidate functional variants that likely modify AD risk by regulating gene expression in myeloid cells. In the MS4A locus we identified a single candidate functional variant and validated it in human induced pluripotent stem cell (hiPSC)-derived microglia and brain. Taken together, this study integrates AD GWAS with multiple myeloid genomic datasets to investigate the mechanisms of AD risk alleles and nominates candidate functional variants, regulatory elements and genes that likely modulate disease susceptibility.This study integrates Alzheimer’s disease (AD) GWAS data with myeloid cell genomics, and reports that myeloid active enhancers are most burdened by AD risk alleles. The authors also nominate candidate causal regulatory elements, variants and genes that likely modulate the risk for AD.
ArticleNumber 1610
Author Kapoor, Manav
Abud, Edsel M.
Fullard, John F.
TCW, Julia
Liu, Yiyuan
Goate, Alison M.
Cheng, Haoxiang
Novikova, Gloriia
Roussos, Panos
Chen, Steven X.
Poon, Wayne W.
Bendl, Jaroslav
Hao, Ke
Liu, Yunlong
Efthymiou, Anastasia G.
Marcora, Edoardo
Björkegren, Johan LM
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– sequence: 2
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  surname: Kapoor
  fullname: Kapoor, Manav
  organization: Ronald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount Sinai, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai
– sequence: 3
  givenname: Julia
  orcidid: 0000-0002-3054-9374
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  givenname: Haoxiang
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Y Lavin (21823_CR20) 2014; 159
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A Nott (21823_CR46) 2019; 366
J Yang (21823_CR41) 2012; 44
Z Tang (21823_CR47) 2015; 163
J Schneppenheim (21823_CR62) 2013; 210
Y Zhang (21823_CR76) 2008; 9
HK Finucane (21823_CR13) 2018; 50
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C Giambartolomei (21823_CR29) 2014; 10
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Z Zhu (21823_CR14) 2016; 48
D Gosselin (21823_CR21) 2014; 159
SH Park (21823_CR36) 2017; 18
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MW Feinberg (21823_CR44) 2007; 26
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AA Nugent (21823_CR71) 2020; 105
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B Soskic (21823_CR72) 2019; 51
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J Hasselmann (21823_CR53) 2019; 103
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BN Vardarajan (21823_CR4) 2015; 77
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Snippet Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer’s disease (AD), but the causal variants, regulatory...
Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer's disease (AD), but the causal variants, regulatory...
This study integrates Alzheimer’s disease (AD) GWAS data with myeloid cell genomics, and reports that myeloid active enhancers are most burdened by AD risk...
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SubjectTerms 631/114/2785
631/208/191
631/378/1689/1283
631/378/371
Alleles
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer's disease
Annotations
Datasets
Enhancers
Gene expression
Gene Expression Regulation
Gene mapping
Gene regulation
Genes
Genetic Predisposition to Disease - genetics
Genetics
Genome-wide association studies
Genome-Wide Association Study
Genomics
Health risks
Humanities and Social Sciences
Humans
Induced Pluripotent Stem Cells - metabolism
Loci
Macrophages
Microglia
Microglia - metabolism
Monocytes
multidisciplinary
Myeloid Cells
Neurodegenerative diseases
Nominations
Pathogenesis
Pluripotency
Regulatory sequences
Regulatory Sequences, Nucleic Acid - genetics
Risk
Science
Science (multidisciplinary)
Stem cells
Transcriptome
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Title Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes
URI https://link.springer.com/article/10.1038/s41467-021-21823-y
https://www.ncbi.nlm.nih.gov/pubmed/33712570
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https://pubmed.ncbi.nlm.nih.gov/PMC7955030
http://kipublications.ki.se/Default.aspx?queryparsed=id:146090939
https://doaj.org/article/e7ee804a940645c0aa0e698c50c1d0da
Volume 12
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