Furthermore, PGC-1α suppresses the transport of NF-κB p65 from the cytoplasm to the nucleus and the degradation of IκBα by regulating NF-κB, thereby reducing Aβ-induced neuronal death and inhibiting neuroinflammation, which in turn reduces mitochondrial damage and restores AD cognitive deficits (Zhang Y. et al., 2017). This evidence concerns the gene PPARGC1A and Alzheimer disease.