Cerebrovascular deposition of amyloid β-protein (Aβ) is a common pathological feature of
Alzheimer's disease and related disorders. In particular, the Dutch E22Q and Iowa D23N
mutations in Aβ cause familial cerebrovascular amyloidosis with abundant diffuse amyloid
plaque deposits. Both of these charge-altering mutations enhance the fibrillogenic and
pathogenic properties of Aβ in vitro. Here, we describe the generation of several transgenic
mouse lines (Tg-SwDI) expressing human neuronal Aβ precursor protein (AβPP) harboring …