*Correspondence: Silke Keiner, [email protected] This article was submitted to Neurogenesis, a section of the journal Frontiers in Neuroscience Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers
1 Introduction Sepsis-associated encephalopathy (SAE) represents a severe complication of sepsis, defined by diffuse brain dysfunction without direct central nervous system (CNS) infection ( Oxidative stress is central to SAE pathogenesis, driven by an imbalance between excessive reactive oxygen species (ROS) production and impaired antioxidant defense systems ( The antioxidant defense system, especially GSH metabolism, is linked to neurodegenerative diseases ( Proteomics and metabolomics enable systematic profiling of protein expression and metabolic signatures
Without adequate collagen production, mineral deposition lacks its structural framework
After the 15 th week of the study, four of the 24 patients in the glutathione group went on to develop neurotoxicity compared to 16 of 18 still reporting neurotoxicity in the placebo group
