This possibility is supported by previous findings by others of a hyperactive phenotype in APOE4 neurons (Nuriel et al., 2017) that in the human brain may lead to accumulation of AD pathological proteins, resulting in the brain hypometabolism that is commonly observed in APOE4 carriers (Langbaum et al., 2010; Nuriel et al., 2017; Reiman et al., 2005). This evidence concerns the gene APOE and Alzheimer disease.