The APOE isoforms differentially shape the transcriptomic and epigenomic landscapes of human microglia xenografted into a mouse model of Alzheimer’s disease

Abstract Microglia play a key role in the response to amyloid beta in Alzheimer’s disease (AD). In this context, the major transcriptional response of microglia is the upregulation of APOE, the strongest late-onset AD risk gene. Of its three isoforms, APOE2 is thought to be protective, while APOE4 i...

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Main Authors: Kitty B. Murphy, Di Hu, Leen Wolfs, Susan K. Rohde, Gonzalo Leguía Fauró, Ivana Geric, Renzo Mancuso, Bart De Strooper, Sarah J. Marzi
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-60099-4
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author Kitty B. Murphy
Di Hu
Leen Wolfs
Susan K. Rohde
Gonzalo Leguía Fauró
Ivana Geric
Renzo Mancuso
Bart De Strooper
Sarah J. Marzi
author_facet Kitty B. Murphy
Di Hu
Leen Wolfs
Susan K. Rohde
Gonzalo Leguía Fauró
Ivana Geric
Renzo Mancuso
Bart De Strooper
Sarah J. Marzi
author_sort Kitty B. Murphy
collection DOAJ
description Abstract Microglia play a key role in the response to amyloid beta in Alzheimer’s disease (AD). In this context, the major transcriptional response of microglia is the upregulation of APOE, the strongest late-onset AD risk gene. Of its three isoforms, APOE2 is thought to be protective, while APOE4 increases AD risk. We hypothesised that the isoforms change gene regulatory patterns that link back to biological function by shaping microglial transcriptomic and chromatin landscapes. We use RNA- and ATAC-sequencing to profile gene expression and chromatin accessibility of human microglia xenotransplantated into the brains of male APP NL-G-F mice. We identify widespread transcriptomic and epigenomic differences which are dependent on APOE genotype and are corroborated across the profiling assays. Our results indicate that impaired microglial proliferation, migration and immune responses may contribute to the increased risk for late-onset AD in APOE4 carriers, while increased phagocytic capabilities and DNA-binding of the vitamin D receptor in APOE2 microglia may contribute to the isoform’s protective role.
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issn 2041-1723
language English
publishDate 2025-05-01
publisher Nature Portfolio
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series Nature Communications
spelling doaj-art-9278e8fccb944ed185b13eaa25e095272025-08-20T03:16:47ZengNature PortfolioNature Communications2041-17232025-05-0116111510.1038/s41467-025-60099-4The APOE isoforms differentially shape the transcriptomic and epigenomic landscapes of human microglia xenografted into a mouse model of Alzheimer’s diseaseKitty B. Murphy0Di Hu1Leen Wolfs2Susan K. Rohde3Gonzalo Leguía Fauró4Ivana Geric5Renzo Mancuso6Bart De Strooper7Sarah J. Marzi8UK Dementia Research Institute at Imperial College LondonUK Dementia Research Institute at Imperial College LondonVIB Center for Brain & Disease Research, VIBVIB Center for Brain & Disease Research, VIBVIB Center for Molecular Neurology, VIBVIB Center for Brain & Disease Research, VIBVIB Center for Molecular Neurology, VIBVIB Center for Brain & Disease Research, VIBDepartment of Brain Sciences, Imperial College LondonAbstract Microglia play a key role in the response to amyloid beta in Alzheimer’s disease (AD). In this context, the major transcriptional response of microglia is the upregulation of APOE, the strongest late-onset AD risk gene. Of its three isoforms, APOE2 is thought to be protective, while APOE4 increases AD risk. We hypothesised that the isoforms change gene regulatory patterns that link back to biological function by shaping microglial transcriptomic and chromatin landscapes. We use RNA- and ATAC-sequencing to profile gene expression and chromatin accessibility of human microglia xenotransplantated into the brains of male APP NL-G-F mice. We identify widespread transcriptomic and epigenomic differences which are dependent on APOE genotype and are corroborated across the profiling assays. Our results indicate that impaired microglial proliferation, migration and immune responses may contribute to the increased risk for late-onset AD in APOE4 carriers, while increased phagocytic capabilities and DNA-binding of the vitamin D receptor in APOE2 microglia may contribute to the isoform’s protective role.https://doi.org/10.1038/s41467-025-60099-4
spellingShingle Kitty B. Murphy
Di Hu
Leen Wolfs
Susan K. Rohde
Gonzalo Leguía Fauró
Ivana Geric
Renzo Mancuso
Bart De Strooper
Sarah J. Marzi
The APOE isoforms differentially shape the transcriptomic and epigenomic landscapes of human microglia xenografted into a mouse model of Alzheimer’s disease
Nature Communications
title The APOE isoforms differentially shape the transcriptomic and epigenomic landscapes of human microglia xenografted into a mouse model of Alzheimer’s disease
title_full The APOE isoforms differentially shape the transcriptomic and epigenomic landscapes of human microglia xenografted into a mouse model of Alzheimer’s disease
title_fullStr The APOE isoforms differentially shape the transcriptomic and epigenomic landscapes of human microglia xenografted into a mouse model of Alzheimer’s disease
title_full_unstemmed The APOE isoforms differentially shape the transcriptomic and epigenomic landscapes of human microglia xenografted into a mouse model of Alzheimer’s disease
title_short The APOE isoforms differentially shape the transcriptomic and epigenomic landscapes of human microglia xenografted into a mouse model of Alzheimer’s disease
title_sort apoe isoforms differentially shape the transcriptomic and epigenomic landscapes of human microglia xenografted into a mouse model of alzheimer s disease
url https://doi.org/10.1038/s41467-025-60099-4
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