Epidermal growth factor prevents oligomeric amyloid- induced angiogenesis deficits invitro

Cerebrovascular dysfunction is a critical component of Alzheimer's disease (AD) pathogenesis. Oligomeric amyloid-42 (oA42) is considered a major contributor to AD progression. However, data are limited on the role of oA42 in brain endothelial cell vessel degeneration/angiogenesis, including the interaction with angiogenic mediators. Thus, the current study determined the effect of oA42 on angiogenesis invitro, utilizing single brain endothelial cell cultures and triple cultures mimicking the microvascular unit (MVU: brain endothelial cells, astrocytes, and pericytes). oA42 dose-dependently reduced angiogenesis and induced vessel disruption. Critically, epidermal growth factor prevented oA42-induced deficits, implicating angiogenic pathways as potential therapeutics for AD.