Therefore we aged four female genetically distinct groups (Tg2576, Tg2576:sod2, sod2+/−, and wild-type controls) on the same genetic background as the Tg2576 mice (F1 C57BL/6J: SJL hybrids), to approximately 16 months of age (when brain amyloid pathology is uniformly well-established in the Tg2576 model [20]) in order to investigate the effects of increased mitochondrial oxidative stress on amyloid and potential tau pathology. Here, MAPT is linked to amyloidosis.