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. 2024 Jan 23;13:7. doi: 10.1186/s40035-024-00397-x

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Cellular hallmarks of ageing in AD, including cellular senescence, disabled macroautophagy, stem cell exhaustion and altered intercellular communication. ROS activated by Aβ and tau can cause stress-induced cellular senescence [10, 152]. The senescent cells exhibit significant dysfunction and abnormal intercellular communication. Ageing microglia release more pro-inflammatory factors and have impaired phagocytic function [153]. Simultaneously, stem cell exhaustion inhibits the transformation of stem cells into neurons, astrocytes and oligodendrocytes [154]. AD Alzheimer’s disease, ROS reactive oxygen species, P16^INK4a a marker of cellular senescence