Fig. 1

The structure of BBB in in vivo A and in vitro B conditions. Brain ECs covers the luminal surface of the BBB interface and are in close contact with blood components. ECs are juxtaposed tightly via the activity of tight junctions, resulting in the formation of a selective barrier interface. ECs are laid on the basal membrane layer which is wrapped by pericytes. Pericytes are sandwiched between ECs at the luminal surface and astrocyte endfeet at the abluminal face. Under pathological conditions, the continuity of the BBB interface is disrupted, leading to the loosening of EC‒to‒EC and EC‒to‒pericyte connections. The production of glycocalyx is not normal on the luminal surface and ECs exhibit several protrusions. Astrocyte endfeet are swollen and lost integrity with pericytes. Along with these changes, the function of several transporters such as cationic amino acid transporter-1 (Cat-1), etc. is disrupted. The increase of adhesion molecules such as VCAM-1 increases the probability of immune cell recruitment and entry via the BBB. The up-regulation of inflammatory cytokines contributes to the abnormal function of tight junction molecules and BBB leakage. Reprinted with permission [18], Copyright 2022. Fluids and Barriers of the CNS