We have used a combination of histological and biochemical methods to analyse the relationships between late-life (after 65 years) SBP and DBP, Alzheimer’s disease pathology (Aβ and tau), non-amyloid small vessel disease (arteriolosclerosis) and cerebral amyloid angiopathy, and markers of cerebral vascular function: ante-mortem cerebral oxygenation [vascular endothelial growth factor-A (VEGF-A) and myelin-associated glycoprotein:proteolipid protein-1 (MAG:PLP1)], BBB integrity [fibrinogen (FGA)] and pericyte content [platelet-derived growth factor receptor β (PDGFRB)]. This evidence concerns the gene PLP1 and early-onset autosomal dominant Alzheimer disease.