Upon exposure of acute hypoxia, microglial activation in the hippocampus of APPswe/PS1dE9 transgenic mice favoured M1 activation and attenuated M2 activation, concurrently, which resulted in the release of pro-inflammatory cytokines and chemokines, such as IL-6, TNF-α, CCL2 and CCL3, and contributed to the pathogenesis of AD, that is hypoxia-induced neuroinflammation (Zhang et al., 2017). This evidence concerns the gene IL6 and Alzheimer disease.