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Through integrated proteomic and metabolomic analyses, we identified a high-inflammation, high-oxidation, low-metabolism triad in the hippocampus of CLP-induced SAE mice, providing novel insights into mechanisms underlying persistent cognitive deficits in SAE survivors

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The process through which NAION destroys vision involves these sequential pathological events: Sudden blood supply disruption: Short posterior ciliary arteries feeding the optic nerve become blocked or experience severe flow reduction, starving nerve tissue Immediate nerve tissue death: Ischemic damage kills optic nerve cells within hours once dead, these neurons cannot regenerate Compartment syndrome: Initial swelling compresses remaining healthy nerve fibers in the confined scleral canal space, creating cascading damage Permanent structural changes: The optic nerve develops atrophy, with dead tissue replaced by glial scarring unable to transmit visual signals NAION commonly affects individuals with crowded optic discs or disc at risk, where cup-to-disc ratio measures 0.2 or less

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