Distinct amyloid-β and tau-associated microglia profiles in Alzheimer’s disease
Open accessAbstract
Alzheimer’s disease (AD) is the most prevalent form of dementia and is characterized by abnormal extracellular aggregates of amyloid-β and intraneuronal hyperphosphorylated tau tangles and neuropil threads. Microglia, the tissue-resident macrophages of the central nervous system (CNS), are important for CNS homeostasis and implicated in AD pathology. In amyloid mouse models, a phagocytic/activated microglia phenotype has been identified. How increasing levels of amyloid-β and tau pathology affect human microglia transcriptional profiles is unknown. Here, we performed snRNAseq on 482,472 nuclei from non-demented control brains and AD brains containing only amyloid-β plaques or both amyloid-β plaques and tau pathology. Within the microglia population, distinct expression profiles were identified of which two were AD pathology-associated. The phagocytic/activated AD1-microglia population abundance strongly correlated with tissue amyloid-β load and localized to amyloid-β plaques. The AD2-microglia abundance strongly correlated with tissue phospho-tau load and these microglia were more abundant in samples with overt tau pathology. This full characterization of human disease-associated microglia phenotypes provides new insights in the pathophysiological role of microglia in AD and offers new targets for microglia-state-specific therapeutic strategies.
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AD1 cluster closely reassembled mouse DAM/MGnD phenotype and was only abundant in human samples containing Aβ and not tau.
“a population of clusters, namely AD1, closely reassembled the mouse DAM/MGnD phenotype, it was only abundant in human samples containing Aβ and not tau”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [119]
The Results section reports that AD1 microglia resemble the phagocytic/activated DAM profile seen in amyloid mouse models. It finds a strong correlation between AD1 abundance and amyloid-β load only in samples without detectable tau pathology, but it does not say AD1 is abundant only in those samples: AD1 microglia were also present, at a lower proportion, in samples with both pathologies. The claim turns a conditional correlation into an exclusive presence claim. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThere exist other microglial subsets in AD besides DAM/MGnD; human microglia are heterogeneous, limiting translation of DAM signature from animal models.
“Together this work demonstrates, firstly, that there exist other microglial subsets in AD besides the DAM/MGnD phenotype, and secondly, that human microglia are heterogenous, thus limiting the translation of the DAM signature from animal models.”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [119]
The Discussion (page unavailable) identifies two distinct human AD-associated microglial profiles: AD1 resembles the phagocytic/activated profile in amyloid mouse models, while AD2 is a different, tau-associated profile. This supports the existence of human microglial subsets beyond DAM/MGnD, but the paper does not establish that heterogeneity limits translation of the DAM signature from animal models; it reports a similarity between mouse and human AD1 microglia. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTwo recent reports suggest the presence of B cells in the brains of patients with AD.
“These findings were not formally published, however two recent reports suggest the presence of B cells in the brains of patients with AD [81,82].”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [82]
The Results section ('Enrichment of less abundant CNS cell types by depletion of neurons and oligodendrocytes/OPCs'; page unavailable) identifies a lymphocyte cluster in brain samples that included AD donors. The paper does not explicitly identify those lymphocytes as B cells, so it supports the presence of lymphocytes in AD brains but not the claim’s more specific cell type. (LLM, conf=0.82)
Experimental — accuracy not yet measuredA study using single-nucleus RNA sequencing identified a cluster of lymphocytes in AD brains enriched for expression of IL-7R and MS4A1 genes, encoding IL-7 receptor and CD20, both established markers of B lymphocytes.
“A study using singlenucleus RNA sequencing identified a cluster of lymphocytes in AD brains enriched for the expression of IL-7R and MS4A1 genes, which encode the interleukin-7 receptor and CD20 respectively, both estab lished markers of B lymphocytes [82].”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [82]
The Results section on enrichment of less abundant CNS cell types reports that single-nucleus RNA sequencing identified a lymphocyte cluster enriched for IL7R and MS4A1 expression in samples that included AD brains. Our copy does not state that these genes encode the named proteins or that both are established B-lymphocyte markers. It also says the clusters were present in all samples, not only AD samples. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThere was considerable overlap between the Micro_D profile and previously reported microglial states, such as MIMS-foamy, amyloid-associated microglia in Alzheimer's disease and lipid-associated macrophages in obesity.
“There was considerable overlap between the Micro_D profile and previously reported microglial states, such as the MIMS-foamy state reported in ref. 11, amyloid-associated microglia in Alzheimer’s disease43,46,47 and lipid-associated macrophages (LAMs) in obesity48 (Extended Data Fig. 8).”
From Foamy microglia link oxylipins to disease progression in multiple sclerosis (2026) · cites this paper as [46]
The foamy, GPNMB+ microglial phenotype in MS lesions bears striking transcriptional similarity to LAMs in obesity, amyloid-responsive microglia in Alzheimer's disease and foam cells in atherosclerosis.
“The foamy, GPNMB+ microglial phenotype in MS lesions bears striking transcriptional similarity to LAMs in obesity, amyloid-responsive microglia in Alzheimer’s disease and foam cells in atherosclerosis18,46,48,50,51.”
From Foamy microglia link oxylipins to disease progression in multiple sclerosis (2026) · cites this paper as [46]
Single nuclei RNA sequencing on AD brains showed gene expression changes only in microglia out of seven cell types.
“single nuclei RNA sequencing on AD brains showed that out of seven cell types, gene expression changes were shown only in microglia [119]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [119]
AD2 did not overlap with AD1 and was more frequently observed in human brain samples with both tau and amyloid pathology.
“AD2 did not overlap with AD1 and was more frequently observed in human brain samples showing both tau and amyloid pathology [119]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [119]
Single cell nuclei extraction from frozen human brain tissue revealed 13 distinct microglial clusters.
“single cell nuclei extraction from frozen human brain tissue revealed 13 distinct microglial clusters [119]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [119]
Distinct Aβ and tau-associated microglia signatures have been discovered in AD patients.
“Moreover, distinct Aβ and tau-associated microglia signatures have been discovered in AD patients.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [15]
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Human Microglia Show Unique Transcriptional Changes in Alzheimer's Disease
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Microglial mechanisms drive amyloid-β clearance in immunized patients with Alzheimer’s disease
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Immune Activation in Alzheimer Disease
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“Within the microglia population, two distinct expression profiles were recently identified, associated with either Aβ load or tissue phosphorylated tau (ptau).(11) Colocalization of tau and activated microglia was demonstrated,(12,13) and Aβ plaque-dependent microglia was identified.”
Towards PET imaging of the dynamic phenotypes of microglia
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Ferroptosis mechanism and Alzheimer's disease
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Tracking cell-type-specific temporal dynamics in human and mouse brains
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An emerging role for microglia in stress‐effects on memory
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Multimodal Omics Approaches to Aging and Age-Related Diseases
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Monocyte-derived macrophages act as reinforcements when microglia fall short in Alzheimer’s disease
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Utilising Induced Pluripotent Stem Cells in Neurodegenerative Disease Research: Focus on Glia
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Decoding Aging Hallmarks at the Single-Cell Level
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Microglial phagocytosis in Alzheimer disease
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- Authors
- Gerrits, E., Brouwer, N., Kooistra, S. M., Woodbury, M. E., Vermeiren, Y., Lambourne, M., Mulder, J., Kummer, M., Möller, T., Biber, K., Dunnen, W. F. A. D., De Deyn, P. P., Eggen, B. J. L., & Boddeke, E. W. G. M.
- Affiliations
- University Medical Center Groningen (NL)
- AbbVie (United States) (US)
- Karolinska Institutet (SE)
- AbbVie (Germany) (DE)
- University of Copenhagen (DK)
- Corresponding author
- Boddeke, Erik W. G. M.
- ORCID
- Venue
- Acta Neuropathologica
- Published
- 2021-02-20
- Volume
- 141
- Issue
- 5
- Pages
- 681-696
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- PMC
- PMC8043951
- OpenAlex
- W3129453843
- Cited by
- 441
- References
- 42
- Citations by year
- 2026: 69 · 2025: 80 · 2024: 124 · 2023: 53 · 2022: 87 · 2021: 27 · 2012: 1
- FWCI
- 30.05
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Acta Neuropathologica (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, cc-by)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion, cc-by)
- Socio-Environmental Systems Modeling (acceptedVersion, cc-by)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, cc-by)
- Data Archiving and Networked Services (DANS) (submittedVersion, cc-by)
- Funders
- Rijksuniversiteit Groningen
- Stichting MS Research
- Fonds Wetenschappelijk Onderzoek (12Z1620N)
- Universitair Medisch Centrum Groningen
- Vlaamse Instelling voor Technologisch Onderzoek
- Alzheimer Nederland
- Vlaamse regering
- 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
- Alzheimer's disease, microglia, amyloid plaques, tau pathology, microglial activation, microglial phenotype, single-nucleus RNA sequencing, phosphorylated tau, disease-associated microglia, microglia-targeted therapy
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain, Female, Humans, Male, Amyloid beta-Peptides, tau Proteins, Microglia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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