Aβ12-28 P treatment in an amyloid mouse model with apoE2-TR or apoE4-TR mouse background resulted in Aβ oligomer and plaque load reduction and alleviated neuritic degeneration indicating that inhibition of Aβ/apoE interaction appears to effectively block aggregation and deposition of Aβ, regardless of apoE isoform20. This evidence concerns the gene APOE and amyloidosis.