IL1B and Cognitive impairment: The possible reason could be that: 1) elevated serum ATG5 dysregulates autophagic flux, resulting in neuronal loss (31); 2) excessive serum ATG5 contributes to ferroptosis in brain IRI, thus promoting ischemic damage (12); 3) serum ATG5 regulates secretion of mature IL-1β and prevent its degradation (32), which is involved in vascular cognition impairment (33); and 4) according to the findings of this study, serum ATG5 level was positively correlated with Th17 cells, and Th17 cells might aggravate cognition impairment by promoting neural inflammation and apoptosis (22-, , 25,27).