Cited by 204Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsAutophagy in Disease and Therapy

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Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence

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Choi, Insup, Wang, Minghui, Yoo, Seungyeul, Xu, Peng, Seegobin, Steven P., Li, Xianting, Han, Xian, Wang, Qian, Peng, Junmin, Zhang, Bin, Yue, Zhenyu·2023·Nature Cell Biology

DOI 10.1038/s41556-023-01158-0PMC PMC10950302

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Abstract

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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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: Choi, Insup
Wang, Minghui
Yoo, Seungyeul
Xu, Peng
Seegobin, Steven P.
Li, Xianting
Han, Xian
Wang, Qian
Peng, Junmin
Zhang, Bin
Yue, Zhenyu
Venue: Nature Cell Biology
Publisher: Springer Science and Business Media LLC
Published: 2023-05-25
Volume: 25
Issue: 7
Pages: 963-974
ISSN: 1465-7392 (ISSN-L)
1476-4679
DOI: 10.1038/s41556-023-01158-0
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: www.springernature.com/gp/researchers/text-and-data-mining (tdm)
www.springernature.com/gp/researchers/text-and-data-mining (vor)
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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Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence

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