Nature Communications (Mar 2021)
Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes
- 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
Affiliations
- Gloriia Novikova
- Ronald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount Sinai
- Manav Kapoor
- Ronald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount Sinai
- Julia TCW
- Ronald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount Sinai
- Edsel M. Abud
- Department of Neurobiology & Behavior, University of California Irvine
- Anastasia G. Efthymiou
- Ronald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount Sinai
- Steven X. Chen
- Department of Medical and Molecular Genetics, Indiana University School of Medicine
- Haoxiang Cheng
- Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai
- John F. Fullard
- Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai
- Jaroslav Bendl
- Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai
- Yiyuan Liu
- Ronald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount Sinai
- Panos Roussos
- Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai
- Johan LM Björkegren
- Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai
- Yunlong Liu
- Department of Medical and Molecular Genetics, Indiana University School of Medicine
- Wayne W. Poon
- Institute for Memory Impairments and Neurological Disorders, University of California Irvine
- Ke Hao
- Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai
- Edoardo Marcora
- Ronald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount Sinai
- Alison M. Goate
- Ronald M. Loeb Center for Alzheimer’s Disease, Department of Neuroscience, Icahn School of Medicine at Mount Sinai
- DOI
- https://doi.org/10.1038/s41467-021-21823-y
- Journal volume & issue
-
Vol. 12,
no. 1
pp. 1 – 14
Abstract
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.
