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.
Main Authors: | , , , , , , , , , , , , , , , , |
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Format: | Article |
Language: | English |
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Nature Portfolio
2021-03-01
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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. |
first_indexed | 2024-12-14T15:17:10Z |
format | Article |
id | doaj.art-e7ee804a940645c0aa0e698c50c1d0da |
institution | Directory Open Access Journal |
issn | 2041-1723 |
language | English |
last_indexed | 2024-12-14T15:17:10Z |
publishDate | 2021-03-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Nature Communications |
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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