Studies revealed that overexpression of PGC-1α suppressed the basal transcription of endogenous BACE1 mRNA (Wang et al., 2013),which further explains the phenomenon that levels of PGC-1α protein are inversely linked to both AD-type neuritic plaque abnormalities and Aβ content (Pohland et al., 2018). This evidence concerns the gene PPARGC1A and Alzheimer disease.