CASP3 and Alzheimer disease: Since Aβ oligomeric aggregates have also been shown to induce caspase-3 activation in neurovascular cells, including endothelial, glial, and neuronal cells (10, 13–15, 206–208), the presence of Aβ deposits surrounding cerebral vessels in AD and CAA, promoting caspase-3 activation, may also prompt an increase in the levels of caspase-3 truncated tau, which is more prone to phosphorylation and aggregation, and may therefore enhance tau toxicity at the NVU (270).