[Dysfunction of the blood-brain barrier during ischaemia: a therapeutic concern]

Since it was discovered and its brain-protective role characterized, the blood-brain barrier (BBB), through the permeability-restricting action of the brain capillary endothelial cells, has been representing a hurdle for 95% of new medical compounds targeting the central nervous system. Recently, a BBB dysfunction is being found in an increasing number of pathologies such as brain ischaemic stroke, whose only therapy consists in a pharmacological thrombolysis limited to a small percentage of the admitted patients, because of the toxical effects of thrombolytics. And since the clinical failure of promising neuroprotectants, numerous studies of brain ischaemia were carried out, with physiopathological or pharmacological approaches refocused on the BBB, whose structural complexity is now expanded to perivascular cells, all forming a functional unit named the neurovascular unit (NVU). Nevertheless, in spite of the numerous molecular mechanisms identified, the process of BBB dysfunction in the ischaemia/reperfusion cascade remains insufficiently established to explain the pleiotropic action exerted by new pharmacological compounds, possibly protecting the entire NVU and representing potential treatments.