Here we show that NF-κB is also over-activated in the CNS following IH, but more importantly, that either NF-κB blockage or a decreased RAGE signaling reduces neuronal degeneration and reactive gliosis, thus demonstrating that RAGE-NF-κB are involved in the detrimental effects observed after IH exposure as a model of SA. This evidence concerns the gene NFKB1 and isolated hemihyperplasia.