There is significant evidence to suggest that a dysfunctional blood-brain barrier [BBB] may contribute to the pathogenesis of some Alzheimer's disease [AD] lesions. An indicator for this could be diminished capillary vascular endothelial growth factor [VEGF] and / or endothelial nitric oxide synthase [eNOS] activity in AD brains. Cortical samples were taken from the superior temporal and calcarine cortices of ten confirmed AD and ten non-demented comparison brains. Contiguous coronal sections were stained using immunohistochemistry techniques to stain for tau protein, beta-amyloid [Abeta] n-termini ([40 & 42]), VEGF and eNOS. Standardized regions of cortex were randomly selected. Areas of ten contiguous field-diameters of comparable and full cortical widths were observed in each section and the densities of neurofibrillary tangles [NFTs], senile plaques [SPs] and Abeta, VEGF and eNOS positive capillaries were recorded. In both AD cortices there were significant inverse correlations found between both VEGF and eNOS-positive microvessels and the presence of NFTs, and each of the amyloid isoforms in SPs and amyloid-positive capillaries [p < 0.01]. In addition there was a significant positive correlation between VEGF and eNOS densities in both cortices [p< 0.01].These results suggest that diminished VEGF and eNOS activity in particularly lesion prone regions of AD brains may contribute to the pathogenesis of NFT and / or SP lesions.