Brain endothelial dysfunction in AD

Increasing evidence suggests that neurovascular dysfunction and neuro‐inflammation is associated with early stages of Alzheimer’s disease (AD). The neuroprotective blood‐brain barrier (BBB) is indispensable for the maintenance of brain homeostasis and proper neuronal functioning. Dysfunction of the BBB and inflammation thereof significantly contributes to the pathogenesis of AD. Amyloid‐β deposition in the microvasculature of the brain, a process referred to as capillary cerebral amyloid angiopathy (capillary CAA), propagates vascular remodeling, which results in impaired function of the blood‐brain barrier and inflammation thereof. While improving vascular function and dampening neuro‐inflammation may be an attractive new way to fight capillary CAA, the underlying factors that mediate vascular alterations in Alzheimer’s disease and capillary CAA pathogenesis remain largely unknown.