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. 2023 Sep 22;8:359. doi: 10.1038/s41392-023-01588-0

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Dysfunctional microglia impair neuronal activity in Alzheimer’s disease. Dysfunctional microglia in AD promotes the clearance of synapses and PNNs and impairs neuronal plasticity and activity. a Microglia harboring an APOE4 allele shows altered cellular metabolism with increased intracellular and extracellular lipid accumulation. The extracellular lipid droplets directly decreased neuronal activity by increasing inward K+ currents. Microglia release Aβ-containing EVs and lead to synaptic dysfunction. Microglial phagocytosis of synapses is affected by astrocytes. Selective removal of astrocytic APOE4 decreases microglial phagocytosis of synaptic elements. b Fibrinogen leaks from the site of cerebrovascular damage into the brain and subsequently binds to the microglial surface receptor CD11b. The interaction of fibrinogen and CD11b mediates microglial activation and leads to spine loss. Microglia engulf perineuronal nets (PNN) and promote plaque-dependent PNN loss. Created with https://BioRender.com