This is evidenced by the higher MAG:PLP1 ratio (see Tayler et al.,42 Barker et al.44, 51 and Miners et al.48,49 and reviewed in Love and Miners77,78) in brain donors with a history of elevated late-life DBP and the lower levels of VEGF-A.47 We previously showed that cerebral hypoperfusion in Alzheimer’s disease is due in part to elevated expression of potent vasoconstrictors, including endothelin-148,79 and angiotensin-II.80,81 Aβ peptides themselves have direct and indirect vasoconstrictor actions.82–85 In contrast, we found no evidence of a relationship between DBP and tangle pathology. The gene discussed is AGT; the disease is early-onset autosomal dominant Alzheimer disease.