In contrast, endothelial production of EDN1, mediated by ECE1 and driven by Aβ40, is more likely to contribute to episodic, free radical‐dependent dysfunction of vascular regulation in AD 48 (Figure 7), including abnormalities of autoregulation and functional hyperaemia demonstrated initially in mouse models of cerebral Aβ accumulation 24, 39 and CAA 49, 54, and more recently in patients with AD 14 and probable CAA 50. This evidence concerns the gene ECE1 and Alzheimer disease.