Yet, although the models exhibit many similarities, they differ in certain aspects, one being the temporal profile of plaque deposition. For example, TgCRND8 mice, which express multiple APP mutations, exhibit parenchymal amyloid deposition as early as 3 months of age.17 APP23 mice, in which a Thy-1 promoter is used to drive expression of the Swedish mutation, are notable for their prominent vascular amyloid deposition and resultant congophilic angiopathy.18 PDAPP and Tg2576 mice also differ in some aspects; for example, in Tg2576 mice, both Aβ40 and Aβ42 are increased more or less proportionately, whereas in PDAPP mice, Aβ42 is disproportionately elevated.16,19 In Tg2576 mice, most amyloid deposits in dense cored plaques, and Tg2576 mice have relatively few of the diffuse deposits found in PDAPP mice. Tg2576 mice are also known for their giant plaques20 and exhibit more vascular amyloid deposition,19 which is largely absent in PDAPP mice.
