The DOI matches its Crossref record; 76 of the 76 references it cites were found in a registry or an index.
Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence
Open accessAbstract
Dysfunctional autophagy has been implicated in the pathogenesis of Alzheimer's disease (AD). Previous evidence suggested disruptions of multiple stages of the autophagy-lysosomal pathway in affected neurons. However, whether and how deregulated autophagy in microglia, a cell type with an important link to AD, contributes to AD progression remains elusive. Here we report that autophagy is activated in microglia, particularly of disease-associated microglia surrounding amyloid plaques in AD mouse models. Inhibition of microglial autophagy causes disengagement of microglia from amyloid plaques, suppression of disease-associated microglia, and aggravation of neuropathology in AD mice. Mechanistically, autophagy deficiency promotes senescence-associated microglia as evidenced by reduced proliferation, increased Cdkn1a/p21 Cip1, dystrophic morphologies and senescence-associated secretory phenotype. Pharmacological treatment removes autophagy-deficient senescent microglia and alleviates neuropathology in AD mice. Our study demonstrates the protective role of microglial autophagy in regulating the homeostasis of amyloid plaques and preventing senescence; removal of senescent microglia is a promising therapeutic strategy.
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“Recent studies have shown that microglial autophagy supports amyloid plaque engagement and helps prevent senescence-associated microglial states [ 62 ].”
From Restores Aβ Clearance by Overcoming PCSK9–LRP1 Dysregulation and TRIB3‐Mediated Autophagy Blockade in Alzheimer's Disease (2026) · cites this paper as [62]
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“A recent report provides evidence that autophagy plays an important role in regulating microglial activation (i.e., DAM phenotype induction)”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [78]
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“deficiency in autophagy leads to senescence, reduces DAMs, impairs Aβ clustering around plaques, and aggravates AD pathology [78].”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [78]
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“Deletion of autophagy gene Atg7 led to impaired ability of microglia to engage Aβ plaques and promoted microglial senescence, which was reversed by administration of senolytic drugs.114”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [114]
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Martinez, J., Malireddi, R. K. S., Lu, Q., Cunha, L. D., Pelletier, S., Gingras, S., Orchard, R., Guan, J.-L., Tan, H., Peng, J., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3192 · Cited by 758
Self-citationRetractedModerated estimation of fold change and dispersion for RNA-seq data with DESeq2
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featureCounts: an efficient general purpose program for assigning sequence reads to genomic features
Liao, Y., Smyth, G. K., & Shi, W. (2014) · Bioinformatics · doi:10.1093/bioinformatics/btt656 · Cited by 27,219
Repertoires of Autophagy in the Pathogenesis of Ocular Diseases
Li, Y., Jiang, Q. L., Cao, G.-F., Yao, J., & Yan, B. (2015) · Cellular Physiology and Biochemistry · doi:10.1159/000373980 · Cited by 16,351
Graph-based genome alignment and genotyping with HISAT2 and HISAT-genotype
Kim, D., Paggi, J. M., Park, C., Bennett, C., & Salzberg, S. L. (2019) · Nature Biotechnology · doi:10.1038/s41587-019-0201-4 · Cited by 15,022
The Molecular Signatures Database Hallmark Gene Set Collection
Liberzon, A., Birger, C., Thorvaldsdóttir, H., Ghandi, M., Mesirov, J. P., & Tamayo, P. (2015) · Cell Systems · doi:10.1016/j.cels.2015.12.004 · Cited by 13,807
Gene Expression Omnibus: NCBI gene expression and hybridization array data repository
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Integrating single-cell transcriptomic data across different conditions, technologies, and species
Butler, A., Hoffman, P., Smibert, P., Papalexi, E., & Satija, R. (2018) · Nature Biotechnology · doi:10.1038/nbt.4096 · Cited by 13,174
Trapnell, C., Cacchiarelli, D., Grimsby, J., Pokharel, P., Li, S., Morse, M., Lennon, N. J., Livak, K. J., Mikkelsen, T. S., & Rinn, J. L. (2014) · Nature Biotechnology · doi:10.1038/nbt.2859 · Cited by 7,314
AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1
Kim, J., Kundu, M., Viollet, B., & Guan, K.-L. (2011) · Nature Cell Biology · doi:10.1038/ncb2152 · Cited by 7,227
Cited by
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Items 201–204 of 204
Zhao, X., He, J., Yu, W., Lin, H., He, Q., Zhenyan, S., & Cheng, S. (2026) · Molecular Neurobiology · doi:10.1007/s12035-026-06281-1
Nemat‐Gorgani, M., Jensen, M. A., & Davis, R. W. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27209351 · Cited by 1
Zi, M., Ye, Q.-Y., Yao, M., Feng, J., Meng, S., Wu, X., Jiang, H., Yang, F., Huang, Y., Hu, X., et al. (2026) · Journal of Alzheimer s Disease · doi:10.1177/13872877261500025
BindingDB (2026) · UC San Diego · doi:10.7270/q2cz3d17
Metadata
- Authors
- Choi, I., Wang, M., Yoo, S., Xu, P., Seegobin, S. P., Li, X., Han, X., Wang, Q., Peng, J., Zhang, B., & Yue, Z.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Sema4 (United States) (US)
- St. Jude Children's Research Hospital (US)
- Corresponding author
- Yue, Zhenyu
- ORCID
- Venue
- Nature Cell Biology
- Published
- 2023-05-25
- Volume
- 25
- Issue
- 7
- Pages
- 963-974
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- PMC
- PMC10950302
- OpenAlex
- W4378212353
- Cited by
- 202
- References
- 76
- Citations by year
- 2026: 49 · 2025: 75 · 2024: 69 · 2023: 9
- FWCI
- 20.92
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- autophagy, microglia, Alzheimer's disease, amyloid plaques, microglial senescence, disease-associated microglia, senescence-associated secretory phenotype, autophagy-lysosome pathway, senolytic therapy, microglial proliferation
- MeSH terms
- Alzheimer Disease, Animals, Autophagy, Disease Models, Animal, Mice, Transgenic, Neurons, Microglia, Mice, Plaque, Amyloid
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