Blood–brain barrier permeability process

The **blood–brain barrier permeability process** describes the ability of molecules, ions, and cells to cross the blood–brain barrier (BBB), a selective barrier formed by endothelial cells, pericytes, and astrocytic end-feet that tightly regulates the movement of substances between the bloodstream and the central nervous system[1][2][3][5]. Permeability is dynamically controlled by **tight junctions**, **transporters**, **endocytic vesicles**, and is influenced by neurological disorders, inflammation, metabolic signals, and external stimuli[3][5]. Disruption or increased permeability of the BBB is a hallmark of various **pathological conditions** (e.g., stroke, neuroinflammation, tumors) and is often exploited pharmacologically to deliver drugs to the brain, though this comes with significant safety concerns[2][3][5]. Key points: - This is a process, not a druggable molecule. - Multiple molecular targets and pathways regulate BBB permeability, including tight junction proteins (claudins, occludin), transporters (GLUT-1, P-glycoprotein), and signaling molecules (VEGF, cytokines)[1][2][3][5]. - Pharmacological modulation of BBB permeability is feasible but is associated with complex risks[2][3][5].

Other names

BBB permeabilityBlood–brain barrier dysfunctionBBB integrity loss

Not applicable as a direct target, but drugs may: Increase paracellular permeability (e.g., by loosening tight junctions); Induce transcytosis; Modulate endothelial transporters and efflux mechanisms (e.g., through P-glycoprotein inhibition)