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

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.

Bibliographic Details
Main Authors: Gloriia Novikova, Manav Kapoor, Julia TCW, Edsel M. Abud, Anastasia G. Efthymiou, Steven X. Chen, Haoxiang Cheng, John F. Fullard, Jaroslav Bendl, Yiyuan Liu, Panos Roussos, Johan LM Björkegren, Yunlong Liu, Wayne W. Poon, Ke Hao, Edoardo Marcora, Alison M. Goate
Format: Article
Language:English
Published: Nature Portfolio 2021-03-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-021-21823-y
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author Gloriia Novikova
Manav Kapoor
Julia TCW
Edsel M. Abud
Anastasia G. Efthymiou
Steven X. Chen
Haoxiang Cheng
John F. Fullard
Jaroslav Bendl
Yiyuan Liu
Panos Roussos
Johan LM Björkegren
Yunlong Liu
Wayne W. Poon
Ke Hao
Edoardo Marcora
Alison M. Goate
author_facet Gloriia Novikova
Manav Kapoor
Julia TCW
Edsel M. Abud
Anastasia G. Efthymiou
Steven X. Chen
Haoxiang Cheng
John F. Fullard
Jaroslav Bendl
Yiyuan Liu
Panos Roussos
Johan LM Björkegren
Yunlong Liu
Wayne W. Poon
Ke Hao
Edoardo Marcora
Alison M. Goate
author_sort Gloriia Novikova
collection DOAJ
description 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.
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spelling doaj.art-e7ee804a940645c0aa0e698c50c1d0da2022-12-21T22:56:16ZengNature PortfolioNature Communications2041-17232021-03-0112111410.1038/s41467-021-21823-yIntegration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genesGloriia Novikova0Manav Kapoor1Julia TCW2Edsel M. Abud3Anastasia G. Efthymiou4Steven X. Chen5Haoxiang Cheng6John F. Fullard7Jaroslav Bendl8Yiyuan Liu9Panos Roussos10Johan LM Björkegren11Yunlong Liu12Wayne W. Poon13Ke Hao14Edoardo Marcora15Alison M. Goate16Ronald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount SinaiRonald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount SinaiRonald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount SinaiDepartment of Neurobiology & Behavior, University of California IrvineRonald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount SinaiDepartment of Medical and Molecular Genetics, Indiana University School of MedicineDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount SinaiDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount SinaiDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount SinaiRonald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount SinaiDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount SinaiDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount SinaiDepartment of Medical and Molecular Genetics, Indiana University School of MedicineInstitute for Memory Impairments and Neurological Disorders, University of California IrvineDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount SinaiRonald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount SinaiRonald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount SinaiThis 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.https://doi.org/10.1038/s41467-021-21823-y
spellingShingle Gloriia Novikova
Manav Kapoor
Julia TCW
Edsel M. Abud
Anastasia G. Efthymiou
Steven X. Chen
Haoxiang Cheng
John F. Fullard
Jaroslav Bendl
Yiyuan Liu
Panos Roussos
Johan LM Björkegren
Yunlong Liu
Wayne W. Poon
Ke Hao
Edoardo Marcora
Alison M. Goate
Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes
Nature Communications
title Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes
title_full Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes
title_fullStr Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes
title_full_unstemmed Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes
title_short Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes
title_sort integration of alzheimer s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes
url https://doi.org/10.1038/s41467-021-21823-y
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