Disruption of the murine apoE gene in AD transgenic models significantly delays the formation of the so-called “dense core” Thio-S–positive amyloid plaques (Bales et al, 1997; Irizarry, Cheung et al, 2000a), even though substantial load of diffuse amyloid and elevated concentrations of soluble Aβ peptides remain in the parenchyma (Irizarry, Rebeck et al, 2000b). This evidence concerns the gene APOE and amyloidosis.