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. 2024 Feb 17;61(9):7092–7108. doi: 10.1007/s12035-024-04003-z

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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/.

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Fig. 3 — Role of GSK-3β in PD: oxidative stress is a central mechanism intricate in the pathogenesis of PD. Dopamine metabolism and mitochondrial dysfunction induce formation of reactive oxygen species (ROS) which causes oxidative stress. Beside, impairment of protein degradation pathway promotes oxidative stress. Activated microglia and GSK-3β accelerate oxidative stress by inhibiting the expression of anti-oxidant proteins such as nuclear factor-related erythroid factor (Nrf2) with inhibition of anti-oxidant response element (ARE)