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. 2023 Sep 9;21:613. doi: 10.1186/s12967-023-04493-w

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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 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 — Mitochondrial dysfunction and its association with neurodegenerative disorders. Several mitochondria abnormalities are characterized by a loss of efficiency in the electron transport chain (ETC) and dysfunction in ATP-synthesis machinery. Reactive oxygen species (ROS) is a consequence of the electron transport process, produced as a by-product of oxidative phosphorylation. Furthermore, structural anomalies might lead to an increased ROS production and the release of mitochondria-derived proapoptotic factors. These free radicals can damage cellular lipids, proteins, and DNA, including mtDNA, which entails dysfunctional mitochondria associated with aging, and essentially, all chronic diseases include neurodegenerative pathologies