Schematic model of how angiogenesis results in the breakdown of the blood–brain barrier (BBB) in Alzheimer’s disease (AD). Impaired cerebral blood flow (CBF) [4–8, 23, 25–28], tight junction (TJ) disruption [21, 22, 67], and disturbances in proteins regulating amyloid beta (Aβ) levels in the brain, such as receptor for advanced glycation products (RAGE) and lipoprotein receptor-related protein 1 (LRP1) [31–38], are factors contributing to elevated Aβ levels and subsequent angiogenesis [24, 48, 61, 67, 70]. Inflammation gives rise to elevated pro-angiogenic cytokines such as vascular endothelial growth factor (VEGF), further promoting vascular remodeling in the AD brain [47, 51–54]. Angiogenesis may also occur as a compensatory response to impaired CBF . These processes lead to further Aβ secretion by endothelial cells, exacerbating angiogenesis and the production of reactive oxygen species (ROS), endothelial damage, and neurotoxicity.