Combined with the observation that aberrant upregulated PLD1 expression and activity was reported in reactive astroglial cells from AD brains, where a physical interaction with amyloid precursor protein (APP) [39] alters the mitochondrial function in the brains of scrapie-infected mice [40] as well as in AD brains [41], we speculate that attenuating PLD1 using VU01 in 12-month-old 3xTg-AD may impinge on APOE-related dyslipidemia that may be another key mechanism that needs to be explored to realize the full therapeutic potential of VU01 as a potential LOAD intervention. This evidence concerns the gene APOE and Alzheimer disease.