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In view of the clinical manifestations and treatment outcomes, both of the disorders can be classified as OCSDs

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Breaking this cycle of neuroinflammation requires therapeutics that can cross the blood-brain barrier and directly quench oxidative stress at the source

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Furthermore, oxidative stress cascades involving ROS, neuroinflammatory pathways such as TLR-4, NFB, and NLRP3 inflammasome-driven pyroptosis, vascular endothelial growth factor signaling, as well as diverse forms of cell death, including organellar dysfunction, autophagy, apoptosis, ferroptosis, and necroptosis, require further research to assess their potential as effective therapeutic targets (130)