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. 2024 Feb 9;56(2):301–310. doi: 10.1038/s12276-024-01176-4

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© The Author(s) 2024

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 — In the aged brain, ASM activity is strongly increased in the endothelial cells that make up the BBB. Brain endothelial ASM induces PP1-mediated ezrin/radixin/moesin dephosphorylation via autocrine and/or paracrine effects and further causes cytoskeletal disassembly and excessive caveolae internalization. Increased caveolae-mediated transcytosis by ASM results in BBB hyperpermeability and blood-derived molecule extravasation into the brain parenchyma, ultimately leading to neuronal cell death.