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Comprehensive single-cell transcriptomic atlas of microglia in Alzheimer’s disease mouse models

Molecular Psychiatry (2026)Cite this article

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Abstract

Microglia are central mediators of neuroinflammation in Alzheimer’s disease (AD), yet conserved microglial states and activation trajectories across AD mouse models remain incompletely defined. Here, we constructed a comprehensive Mouse Microglia Atlas (MoMicA) to resolve conserved subtypes, delineate dynamic trajectories, and identify key regulators associated with AD pathology. We integrated ten single-cell and single-nucleus RNA-sequencing datasets from major AD mouse models, yielding 84,764 microglia for harmonized clustering, co-expression network analysis, and pseudotime inference, complemented by immune staining. Across models, AD was characterized by contraction of homeostatic microglia and marked expansion of DAM. MoMicA further delineated refined homeostatic and disease-associated subpopulations, including different homeostatic microglia subclusters and a stepwise progression from homeostatic microglia through activated response and pre-disease-associated states to disease-associated microglia. Network analysis highlighted lipid metabolism and inflammation as dominant AD-related programs and identified Fabp5 as a central hub gene within a DAM-associated lipid module. Multiplex immunofluorescence confirmed that Fabp5 is induced in Clec7a-positive DAM around amyloid plaques in two amyloidosis models. MoMicA therefore provides a valuable resource for dissecting the mechanistic roles of microglia in the onset and progression of AD.

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Fig. 1: An integrated single-cell atlas (MoMicA) reveals distinct microglial subpopulations in mouse models of Alzheimer’s disease.
Fig. 2: AD pathology drives compositional shifts and subcluster-specific transcriptomic changes in microglia.
Fig. 3: Sub-clustering of homeostatic microglia reveals three functionally distinct subpopulations.
Fig. 4: Sub-clustering the DAM population reveals a spectrum of activation states.
Fig. 5: Trajectory analysis predicts a shift from homeostatic to DAM states, confirmed in plaque-associated microglia.
Fig. 6: hdWGCNA identifies co-expression modules and hub genes associated with microglial states.
Fig. 7: The hub gene Fabp5 in DAM cluster is upregulated in disease-associated microglia surrounding amyloid plaques across ages.
Fig. 8: Spatiotemporal dynamics of Fabp5 expression reveal a plaque-dependent induction mechanism.

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Data availability

The source single-cell transcriptomic data used in this study are publicly accessible through the following accession numbers: Figshare: 19706530; Gene Expression Omnibus (GEO): GSE127892, GSE140510, GSE142267, GSE147495, GSE153895, GSE175546, GSE190607, GSE206114 and GSE224398.

Code availability

Code is available from the corresponding author upon request.

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Acknowledgements

This work was supported by the National Key R&D Program of China (STI2030-Major Projects 2021ZD0202400), Natural Science Foundation of Chongqing, China (CSTB2025NSCQ-GPX0386), the National Key R&D Program of China (ST12030-Major Projects 2021zD0200600), the National Natural Science Foundation Project of China (82201688, 82571748, 82471545, 82401784, 32400850, 82401523, 82501836, 82501469, 82501837), National Reserve Talent Project in the Health and Wellness Sector of Chongqing (HBRC202410, HBRC202417), China Postdoctoral Science Foundation (2024MD754023, 2025MD774171, 2025T180580), the Key Project of the Natural Science Foundation of Chongqing (Chongqing Science and Technology Development Foundation) under Grant No. 2024NSCQ-KJFZZDX0005, and the New Chongqing Youth Innovation Talent Project (Life and Health) under Grant No.2024NSCQ-qncxX0029.

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  1. These authors contributed equally: Ping Liu, Tingfang Sun.

Authors and Affiliations

  1. Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China

    Ping Liu, Tingfang Sun, Jie Yang, Hongrui Li, Wanwan Min, Xingyu Zhou, Ruihan Xiong, Jing Wu, Yu Huang, Yifan Li, Minghao Yuan, Jianping Zhang, Xunmin Tan, Xiaodong Song, Hongsheng Zhang & Peng Zheng

  2. NHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, Chongqing Medical University, Chongqing, China

    Jing Wu & Peng Zheng

  3. Department of Neurobiology, School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China

    Hongsheng Zhang

  4. Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), The First Affiliated Hospital of Chongqing Medical University, Chongqing, China

    Hongsheng Zhang

  5. Department of Psychiatry, College of Medicine, SUNY Upstate Medical University, Syracuse, NY, USA

    Ma-Li Wong

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Contributions

Designed the experiments: PZ. Performed the experiments: PL and TFS. Analyzed the data: JY, HRL, WWM, XYZ, RHX, JW, YH, YFL, MHY, JPZ, XMT, XDS, and HSZ. Drafted the paper: PL and TFS. Revised the paper for intellectual content: PZ and MLW.

Corresponding authors

Correspondence to Ma-Li Wong or Peng Zheng.

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The original studies of single-cell transcriptomic data had obtained the necessary ethical approval for sample collection. This study obtained ethical clearance from the Ethical Committee of Chongqing Medical University (Chongqing, China; IACUC-CQMU-2024-0710).

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Liu, P., Sun, T., Yang, J. et al. Comprehensive single-cell transcriptomic atlas of microglia in Alzheimer’s disease mouse models. Mol Psychiatry (2026). https://doi.org/10.1038/s41380-026-03529-z

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