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. 2023 Apr 18;12(4):955. doi: 10.3390/antiox12040955

Figure 1.

Figure 1

The vicious cycle in Parkinson’s disease, involving alterations in redox homeostasis, dysfunctional mitochondria, and neuroinflammation. Mitochondria are the main site of ROS production, and, at the same time, ROS may affect mitochondrial functionality. Mitochondria can stimulate neuroinflammatory responses through the release of damage-associated molecular patterns (DAMPs). Chronic activation of microglia stimulates the production of ROS through the activation of NADPH oxidase (NOX). In dopaminergic neurons, cytosolic dopamine (DA) can auto-oxidase leading to the generation of ROS and reactive quinones (DAQs), which can either react with cellular nucleophiles or aggregate into neuromelanin (NM). The release of NM from dying neurons can fuel neuroinflammatory processes by activating microglia. Alternatively, cytosolic DA can be metabolized at the mitochondrial level into the very reactive molecule dihydroxyphenylacetaldehyde (DOPAL). The role of the oxidation product of DA in this vicious cycle will be discussed in the following sections. (Created with BioRender.com, accessed on 13 April 2023.)