These transgenic mice overexpress a mutated form of the human amyloid precursor protein (APP) gene with the Swedish mutation (APPswe KM670/671NL), leading to the overproduction of β-amyloid (Aβ) peptides and their accumulation in amyloid plaques, a typical pathological hallmark of AD (Hsiao, 1998). This evidence concerns the gene APP and amyloidosis.