The difference in CAA dependence of α-SMA loss between the arterioles and the arteries (Figs. 2, 3), and the similarities in collagen content between AD, NDCTRL, CAA-, and non-CAA-affected vessels prompted us to study whether Braak tau pathology, independent of CAA and cognitive status of the subjects, might affect the cerebrovascular α-SMA and collagen content in our study population, and whether this might also be vessel type dependent. The gene discussed is MAPT; the disease is Alzheimer disease.