These findings are consistent with PET evidence of lower CMRglc in AD-vulnerable regions among post-menopausal women (Mosconi et al., 2018b, 2021), and provide further support to the notion that a triad of AD risk consisting of age, sex, and APOE4 genotype impacts bioenergetic pathways already in midlife (Riedel et al., 2016), further implicating the importance of mitochondrial alterations for AD risk (Riedel et al., 2016; Wang and Brinton, 2016). This evidence concerns the gene APOE and Alzheimer disease.