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Ischemic damage to brain cells results in the significant release of excitotoxic amino acids triggering immediate oxidative stress response and neuroinflammation, leading to secondary brain damage around the core infarction zone (1416)

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& Holden, J

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Current pharmacological interventions for oxidative stress in the nervous systemsuch as edaravone (15, 16) and N-acetylcysteine (16, 17)act on single targets and employ relatively narrow mechanisms, and are associated with dose-limiting adverse effects and loss-of-benefit phenomena (e.g., end-of-dose deterioration and motor complications), rather than durable disease modification (18)