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Cited by 25Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

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

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Murphy, Kitty B., Hu, Di, Wolfs, Leen, Rohde, Susan K., Fauró, Gonzalo Leguía, Geric, Ivana, Mancuso, Renzo, De Strooper, Bart +1 more·2025·Nature Communications
DOI 10.1038/s41467-025-60099-4PMC PMC12106835
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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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  • E2 expression upregulates genes associated with cellular migration and the immune response in microglia compared to E3 and E4.

    “upregulate genes associated with cellular migration and the immune response in microglia compared to E3 and E4”

    From Older adult APOE4 mice exhibit modest immunometabolic adaptation following microglial APOE2 replacement (2027) · cites this paper as Murphy et al., 2025

    The Results section, “APOE2-expressing microglia are associated with increased cellular migration and phagocytosis” (Fig. 5; page not provided), reports a migration-associated gene module upregulated in APOE2 microglia compared with both APOE3 and APOE4. The immune-response-associated module was upregulated compared with APOE4 only, so the claim's comparison with APOE3 is not supported for immune-response genes. (LLM, conf=0.90)

    Experimental — accuracy not yet measured

  • E2 expression increases phagocytic activity in microglia compared to E3 and E4.

    “E2 expression has been shown to increase phagocytic activity”

    From Older adult APOE4 mice exhibit modest immunometabolic adaptation following microglial APOE2 replacement (2027) · cites this paper as Murphy et al., 2025

  • E2 expression decreases lipid accumulation compared to E3 and E4.

    “decrease lipid accumulation”

    From Older adult APOE4 mice exhibit modest immunometabolic adaptation following microglial APOE2 replacement (2027) · cites this paper as Murphy et al., 2025

    The Results report that TSPAN13, a gene associated with lipid accumulation, is upregulated in APOE4 microglia; the Discussion suggests lipid dysregulation in APOE4 microglia. Neither passage reports lipid accumulation in APOE2 microglia compared with both APOE3 and APOE4. Searches for lipid accumulation and lipid droplets did not establish the claimed comparison. (LLM, conf=0.74)

    Experimental — accuracy not yet measured

  • E2 expression decreases microgliosis compared to E3 and E4.

    “decrease microgliosis”

    From Older adult APOE4 mice exhibit modest immunometabolic adaptation following microglial APOE2 replacement (2027) · cites this paper as Murphy et al., 2025

    The Results section on APOE2-expressing microglia reports a proliferation-associated gene module upregulated in APOE2 compared with APOE3 and APOE4, while the Discussion reports enhanced phagocytic activity. Neither passage measures microgliosis or says that APOE2 decreases it; searches for microgliosis and reduced microglial proliferation or number did not establish the claim. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

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Cited by

Sorted by citations

Authors
Murphy, K. B., Hu, D., Wolfs, L., Rohde, S. K., Fauró, G. L., Geric, I., Mancuso, R., De Strooper, B., & Marzi, S. J.
Affiliations
  • King's College London (GB)
  • UK Dementia Research Institute (GB)
  • VIB-KU Leuven Center for Brain & Disease Research (BE)
  • University of Antwerp (BE)
Corresponding author
Marzi, Sarah J.
ORCID
Venue
Nature Communications
Publisher
Springer Science and Business Media LLC
Published
2025-05-27
Volume
16
Issue
1
Pages
4883-4883
ISSN
2041-1723 (ISSN-L)
DOI
10.1038/s41467-025-60099-4
PMC
PMC12106835
OpenAlex
W4410735111
Cited by
25
References
20
Citations by year
2026: 18 · 2025: 7
FWCI
8.16
Type
journal article
Language
en
Open access
Licence
Locations
  • Nature Communications (publishedVersion, cc-by)
  • bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
  • Lirias (KU Leuven) (submittedVersion, cc-by)
  • RePEc: Research Papers in Economics (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Research Portal (King's College London) (submittedVersion, cc-by)
Funders
  • Alzheimer's Association (ABA-22-968700, E2A-23-1148152, ADSF-21-829660-C)
  • BrightFocus Foundation (A2021034S)
  • National Institute for Health and Care Research
  • European Commission (HORIZON2020, 834682, 2022-2025)
  • Fonds Wetenschappelijk Onderzoek (12P5922N, G0C9219N, G0K9422N, G056022N, 2022-2025)
  • Universiteit Antwerpen (BOF-TOP 2022-2025, 2018-AARF-591110-RAPID, 2018-AARF-591110)
  • UK Dementia Research Institute (UKDRI-6205)
  • Medical Research Council (W004984, MR/W004984/1, MR/Y014847/1)
  • NIHR Imperial Biomedical Research Centre
  • HORIZON EUROPE European Research Council (101041867)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
APOE isoforms, APOE2, APOE ε4, Alzheimer's disease, microglia, transcriptome, chromatin accessibility, epigenomics, amyloid-beta, microglial proliferation, microglial migration, phagocytosis, vitamin D receptor, gene expression regulation
MeSH terms
Alzheimer Disease, Animals, Apolipoproteins E, Brain, Chromatin, Disease Models, Animal, Humans, Male, Mice, Transgenic, Phagocytosis, Microglia, Protein Isoforms, Gene Expression Profiling, Mice, Apolipoprotein E4, Apolipoprotein E2, Epigenomics, Transcriptome

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