Human microglial state dynamics in Alzheimer’s disease progression
Open accessAbstract
Altered microglial states affect neuroinflammation, neurodegeneration, and disease but remain poorly understood. Here, we report 194,000 single-nucleus microglial transcriptomes and epigenomes across 443 human subjects and diverse Alzheimer's disease (AD) pathological phenotypes. We annotate 12 microglial transcriptional states, including AD-dysregulated homeostatic, inflammatory, and lipid-processing states. We identify 1,542 AD-differentially-expressed genes, including both microglia-state-specific and disease-stage-specific alterations. By integrating epigenomic, transcriptomic, and motif information, we infer upstream regulators of microglial cell states, gene-regulatory networks, enhancer-gene links, and transcription-factor-driven microglial state transitions. We demonstrate that ectopic expression of our predicted homeostatic-state activators induces homeostatic features in human iPSC-derived microglia-like cells, while inhibiting activators of inflammation can block inflammatory progression. Lastly, we pinpoint the expression of AD-risk genes in microglial states and differential expression of AD-risk genes and their regulators during AD progression. Overall, we provide insights underlying microglial states, including state-specific and AD-stage-specific microglial alterations at unprecedented resolution.
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Microglial populations in Alzheimer's disease shift dynamically across disease contexts rather than fitting neatly into a few fixed states.
“large human studies have shown that microglial populations in Alzheimer’s disease shift dynamically across disease contexts rather than fitting neatly into a few fixed states”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [22]
Microglia in Alzheimer's disease occupy multiple transcriptional trajectories rather than discrete and permanent categories.
“Large human microglial atlases and state-dynamics studies are beginning to show that microglia in Alzheimer’s disease occupy multiple transcriptional trajectories rather than discrete and permanent categories [22,47].”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [22]
Human microglial states often overlap only partially with mouse-defined categories.
“human microglial states often overlap only partially with mouse-defined categories”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [22]
Microglia from APOE4 mouse models, as well as human microglia from post-mortem brain tissue in AD and APOE4 carriers, exhibit lipid dysregulation and upregulation of neutral lipid storage.
“Microglia from APOE4 mouse models, as well as human microglia from post-mortem brain tissue in AD and APOE4 carriers, exhibit lipid dysregulation and upregulation of neutral lipid storage17,27–29.”
From APOE genotypes differentially remodel the astrocytic lipid droplet proteome to shape lipid droplet dynamics (2026) · cites this paper as [28]
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“…especially important because human microglial states often overlap only partially with mouse-defined categories, and large human studies have shown that microglial populations in Alzheimer’s disease shift dynamically across disease contexts rather than fitting neatly into a few fixed states [22].”
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- Authors
- Sun, N., Victor, M. B., Park, Y. P., Xiong, X., Scannail, A. N., Leary, N., Prosper, S., Viswanathan, S., Luna, X., Boix, C. A., James, B. T., Tanigawa, Y., Galani, K., Mathys, H., Jiang, X., Ng, A. P., Bennett, D. A., Tsai, L.-H., & Kellis, M.
- Affiliations
- Broad Institute (US)
- Massachusetts Institute of Technology (US)
- University of Pittsburgh (US)
- Rush University Medical Center (US)
- Corresponding author
- Tsai, Li-Huei
- Kellis, Manolis
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2023-09
- Volume
- 186
- Issue
- 20
- Pages
- 4386-4403.e29
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC10644954
- OpenAlex
- W4387142551
- Cited by
- 462
- References
- 39
- Citations by year
- 2026: 187 · 2025: 156 · 2024: 107 · 2023: 11 · 2022: 1
- FWCI
- 47.58
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cell (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Cure Alzheimer's Fund
- Howard Hughes Medical Institute
- National Institutes of Health (R01AG17917, AG062335, AG058002, P30AG72975, AG074003, NS127187, MH109978, NS110453, U01AG61356, NS115064, R01AG57473, 1RF1AG054321, R01AG15819, U01AG46152, AG062377, AG054012, AG067151, P30AG10161, AG081017, AG077227, NS129032)
- JPB Foundation
- Robert A. and Renee E. Belfer Family Foundation
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Single-cell and spatial transcriptomics
- Keywords
- Alzheimer's disease, microglial states, neuroinflammation, single-nucleus transcriptomics, epigenomics, gene regulatory networks, transcription factor regulation, disease progression, lipid processing, homeostatic microglia
- MeSH terms
- Epigenome, Alzheimer Disease, Gene Expression Regulation, Humans, Inflammation, Transcription Factors, Microglia, Transcriptome
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