NFKB1 and asthma: In addition, the onset of oxidative stress in asthma regulates the Th1/Th2-type immune inflammatory response, activates microglia, and promotes the release of inflammatory factors in cognitively involved brain regions such as the hippocampus by activating the NF-kB signal pathway, which may diminish N-acetylaspartate (NAA) levels in the hippocampus of patients with asthma and ultimately lead to cognitive dysfunction, including learning and memory (21, 52).