Adipose and leptomeningeal arteriole endothelial dysfunction induced by β-amyloid peptide: a practical human model to study Alzheimer's disease vasculopathy.

Background Evidence point to vascular dysfunction and hypoperfusion as early abnormalities in Alzheimer's disease (AD); probing their mechanistic bases can lead to new therapeutic approaches. We tested the hypotheses that β-amyloid peptide induces endothelial dysfunction and oxidative stress in human microvasculature and that response will be similar between peripheral adipose and brain leptomeningeal arterioles.