Although this may be the case in individualvessels, our unbiased quantitative assessment of the vascular expression of ALK1 in thehippocampal parenchyma—in groups of subjects matched for age, sex, the degree of CAA, andvascular changes as well as the absence of non-AD pathology—indicates that the reduced ALK1signal that accompanies AD progression is a feature of the arterioles in general (Fig. 4), apart from the presence of Aβ in the analyzedvessels or the global CAA evaluation of the subjects documented in the neuropathologyreports. Here, ACVRL1 is linked to Alzheimer disease.