Subsequently, many other transgenic lines were developed with approaches similar to those used to develop PDAPP and Tg2576 mice9–11 typically relying on strong promoters to drive expression of APP transgenes containing single or multiple FAD mutations. Common features of the models have been the production of elevated levels of Aβ, amyloid plaques, dystrophic neurites, and gliosis. Behavioral deficits have been common.10 Many additional neuropathological, electrophysiological, and neurochemical changes that model aspects of AD in humans have also been observed.10
