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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. 1 — Intracellular hallmarks of ageing in AD. The intracellular hallmarks of ageing include genomic instability, macromolecular damage, epigenetic alterations, deregulated nutrient sensing and mitochondrial dysfunction. Additionally, protein damage in AD mainly manifests as the abnormal aggregation of Aβ and tau proteins, which is related to cerebral insulin resistance and affects nutrient sensing in nerve cells [19]. The green arrow indicates that IGF-1R is downregulated in the brain tissues of patients with AD [20]. AD Alzheimer’s disease, ncRNAs non-coding RNAs, lncRNA long non-coding RNA, miRNA microRNA, circRNA circular RNA