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. 2023 Feb 21;8:73. doi: 10.1038/s41392-023-01353-3

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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 — Intracellular α-synuclein homeostasis is maintained via the ubiquitin–proteasome and lysosomal autophagy systems. Impairment of these degradation systems by OS, mitochondrial dysfunction, or neuroinflammation could contribute to α-synuclein accumulation. Furthermore, mutations of genes like LRRK2, DJ-1, Parkin, and Pink1 cause mitochondrial dysfunction and increase cell death. Finally, OS and neuroinflammation appear to be connected