The present study aimed to determine whether the RAGE-specific antibody protects against BBB disruption and cognitive impairment induced by isoflurane exposure in aged rats.
These findings indicated that upregulating RAGE and/or downregulating LRP-1 at the hippocampus and the prefrontal lobe contributed to the Aβ<sub>1-42</sub> accumulation and then further promoted the cognitive impairment of diabetic rats.
Here, we investigated the role of the receptor for advanced glycation end products (RAGE) in neuroinflammation, neurodegeneration-associated changes, and cognitive dysfunction arising after sepsis recovery.
RAGE over-expression in the hippocampal vascular endothelial cells possibly resulted in the excessive transport of the plasma Aβ1-40 into the brain after treatment with sevoflurane, which was associated with sevoflurane-induced cognitive dysfunction in aged mice.