Schelle J, Wegenast-Braun BM, Fritschi SK, et al. - Since Aβ (β-amyloid peptides) have a causal role for cerebral amyloid angiopathy (CAA) and related hemorrhages, and CAA occurs with normal aging and to different degrees in Alzheimer disease, where its influence and management is confounded by the presence of parenchymal Aβ deposition, researchers performed this investigation on the experimental models (mice) and visualized CAA and evaluated Aβ in cerebrospinal fluid and brain, using 3-dimensional ultramicroscopy and immunoassays. APP(Aβ precursor protein)Dutch mice manifest CAA in the absence of parenchymal amyloid, imitating hereditary cerebral hemorrhage with amyloidosis Dutch type (HCHWA-D). They used a β-site amyloid precursor protein cleaving enzyme 1 inhibitor to treat the mice. For the first time ever, it was shown in this study that CAA in the absence of parenchymal amyloid can be largely prevented via Aβ reduction at early disease time points. A preclinical basis for Aβ-reducing treatments in patients at risk of CAA and in presymptomatic HCHWA-D was offered by the findings.