In this trial, we selected Tg2576, which harbors human APP with the Swedish mutation, with overexpression of human PS2 carrying the Volga German Kindred mutation (N141I)48, which increases the ratio of Aβ42 to Aβ40 to accumulate severely amyloid plaques in these double transgenic mice (PS2Tg2576)49. The gene discussed is APP; the disease is amyloidosis.