IL1B and delirium: The SCP2-mediated dysregulation of lipid metabolism may trigger a cascade of neuroinflammatory responses through the related lipid peroxide-NLRP3-IL-1β pathway, ultimately activating microglial cells.46The accumulation of 3-hydroxyoctanoate as a β-oxidation intermediate can induce mitochondrial stress, leading to increased reactive oxygen species production and subsequent activation of the NLRP3 inflammasome.44This neuroinflammatory cascade, combined with oxidative stress and disruption of the blood-brain barrier function, creates a pathophysiological environment conducive to delirium.47