This research gap needs to be closed because the 2 forms have differing neurotoxicity, and there is evidence that alterations in AD-related genes such as TREM2 (triggering receptor expressed on myeloid cells 2) and APOE (apolipoprotein E) alter the net Aβ plaque fibrillarity, which would consecutively bias the relationship between plaque density and Aβ PET binding in vivo (5). This evidence concerns the gene APOE and Alzheimer disease.