Microglia in Alzheimer's disease at single-cell level. Are there common patterns in humans and mice?
Open accessAbstract
Alzheimer’s disease (AD) is characterized by extracellular aggregates of amyloid β peptides, intraneuronal tau aggregates, and neuronal death. This pathology triggers activation of microglia. Because variants of genes expressed in microglia correlate with AD risk, microglial response to pathology plausibly impacts disease course. In mouse AD models, single-cell RNA sequencing (scRNA-seq) analyses delineated this response as progressive conversion of homeostatic microglia into disease-associated microglia (DAM); additional reactive microglial populations have been reported in other models of neurodegeneration and neuroinflammation. We review all of these microglial signatures, highlighting four fundamental patterns: DAM, IFN–microglia, MHC-II microglia, and proliferating microglia. We propose that all reported microglia populations are either just one or a combination, depending on the clustering strategy applied and the disease model. We further review single-nucleus RNA sequencing (snRNA-seq) data from human AD specimens and discuss reasons for parallels and discrepancies between human and mouse transcriptional profiles. Finally, we outline future directions for delineating the microglial impact in AD pathogenesis.
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Many disease-associated microglial programs are spatially enriched around plaques, suggesting microglial state transitions are disease-stage-dependent and anatomically localized.
“Many disease-associated microglial programs are spatially enriched around plaques, which suggests that microglial state transitions are not only disease-stage-dependent but also anatomically localized.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [46]
The 'Innovative approaches for investigating human microglia in AD' section (page unavailable) reports a spatial association between DAM and amyloid plaques, and 'Proliferating microglia' reports Ki67-positive microglia around plaques in 5xFAD mice. The paper also describes changes in microglial states with disease progression, but it does not establish that many distinct microglial programs are spatially enriched around plaques. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMicroglia can express molecules associated with antigen presentation, including MHC class II-related genes and co-stimulatory ligands such as CD80 or CD86, especially under inflammatory conditions.
“They can express molecules associated with antigen presentation, including MHC class II–related genes and co-stimulatory ligands such as CD80 or CD86, especially under inflammatory conditions.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [46]
The section “IFN-I and MHC-II microglia coexist with DAM” (page unavailable) reports microglial expression of MHC-II genes in disease models and increasing expression as pathology progresses. The Conclusions (page unavailable) say MHC-II expressed by microglia in AD may present antigens. Our copy does not report microglial expression of the co-stimulatory ligands CD80 or CD86, so that specific part of the claim is unsupported. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSingle-cell and single-nucleus studies have identified Alzheimer's-associated microglial states enriched for immune activation, antigen-presentation genes, lipid-processing pathways, and inflammatory mediators.
“Single-cell and single-nucleus studies have repeatedly identified Alzheimer ’s-associated microglial states enriched for immune activation, antigen-presentation genes, lipid-processing pathways, and inflammatory mediators.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [46]
Microglia in Alzheimer's disease appear to acquire hybrid programs: they remain tissue-resident myeloid cells but can express genes normally associated with professional antigen presentation, immune communication, and inflammatory coordination.
“Instead, microglia in Alzheimer’s disease appear to acquire hybrid programs: they remain tissue-resident myeloid cells, but they can express genes normally associated with professional antigen presentation, immune communication, and inflammatory coordination.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [46]
At least some plaque-associated microglia may borrow elements of lymphoid signaling logic rather than merely presenting antigen to lymphocytes.
“The recent finding therefore suggests that at least some plaque-associated microglia may borrow elements of lymphoid signaling logic rather than merely presenting antigen to lymphocytes [44,45,46].”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [46]
The Conclusions discuss TREM2 and phagocytic molecules as well as possible MHC-II antigen presentation, and the section on proliferating microglia describes cells around Aβ plaques. Neither those passages nor searches for lymphoid and lymphocyte signaling identify lymphoid signaling logic in plaque-associated microglia. Our copy therefore does not establish the attributed suggestion. (LLM, conf=0.70)
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- Authors
- Chen, Y., & Colonna, M.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Colonna, Marco
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2021-07-22
- Volume
- 218
- Issue
- 9
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC8302448
- OpenAlex
- W3185694768
- Cited by
- 339
- References
- 92
- Citations by year
- 2026: 65 · 2025: 60 · 2024: 85 · 2023: 75 · 2022: 47 · 2021: 6 · 2012: 1
- FWCI
- 6.23
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The Journal of Experimental Medicine (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion, cc-by-nc-sa)
- Funders
- National Institutes of Health (RF1 AG051485, R21 AG059176, RF1 AG059082)
- 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, microglia, disease-associated microglia, microglial activation, single-cell RNA sequencing, single-nucleus RNA sequencing, microglial proliferation, neuroinflammation, amyloid-beta, tau pathology
- MeSH terms
- Aging, Alzheimer Disease, Animals, Histocompatibility Antigens Class II, Disease Models, Animal, Humans, Interferon Type I, Neurons, Gene Expression, Microglia, Mice, Single-Cell Analysis
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