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Excess ROS then activates the NLRP3 inflammasome in microglia, promoting maturation and release of IL-1 ( 4.3 GSH metabolism: a central hub in mid-late SAE The hippocampus, with its high metabolic demands and low antioxidant capacity, is uniquely vulnerable to septic injury ( A Stat1-Gpx3 hub was identified, where TNF-/IL-1-induced Stat1 activation suppresses Nrf2 (confirmed by reduced hippocampal Nrf2)

Moreover, the potential of personalized medicine in managing oxidative stress-related neurodegeneration is gaining momentum: genetic variants in the Nrf2 signaling pathway or SIRT1-mediated deacetylation affecting astrocytic GSH synthesis (e.g., regulating glutamate cysteine ligase catalytic subunit expression), combined with biomarkers like individual GSH levels and Nrf2 activity, could enable tailored interventions

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