Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized 
by the pathological accumulation of amyloid beta (Aβ) peptides and 
neurofibrillary tangles containing hyperphosphorylated neuronal tau protein. AD 
pathology is also characterized by chronic brain inflammation, which promotes 
disease pathogenesis. In this context, the blood-brain barrier (BBB), a highly 
specialized endothelial cell membrane that lines cerebral microvessels, 
represents the interface between neural cells and circulating cells of the 
immune system. The BBB thus plays a key role in the generation and maintenance 
of chronic inflammation during AD. The BBB operates within the neurovascular 
unit (NVU), which includes clusters of glial cells, neurons and pericytes. The 
NVU becomes dysfunctional during AD, and each of its components may undergo 
functional changes that contribute to neuronal injury and cognitive deficit. In 
transgenic animals with AD-like pathology, recent studies have shown that 
circulating leukocytes migrate through the activated brain endothelium when 
certain adhesion molecules are expressed, penetrating into the brain parenchyma, 
interacting with the NVU components and potentially affecting their structural 
integrity and functionality. Therefore, migrating immune system cells in 
cerebral vessels act in concert with the modified BBB and may be integrated into 
the dysfunctional NVU. Notably, blocking the adhesion mechanisms controlling 
leukocyte-endothelial interactions inhibits both Aβ deposition and tau 
hyperphosphorylation, and reduces memory loss in AD models. The characterization 
of molecular mechanisms controlling vascular inflammation and leukocyte 
trafficking could therefore help to determine the basis of BBB dysfunction 
during AD and may lead to the development of new therapeutic approaches.