ABSTRACT
At the cellular level, astrocytes and endothelial cells (EC) form a selectively permeable barrier known as the blood-brain barrier (BBB). The role of the BBB is to serve as a controlled, functioning gateway protecting the brain from systemic influences, while maintaining homeostasis and allowing transport of nourishment to neurons in the parenchyma.1 Tight junctions formed by microvascular endothelial cells, lack of fenestrations, and minimal pinocytic vesicles restrict the diffusion of proteins and other molecules into the intracellular space of the brain. However, under certain conditions, the BBB may have an increased permeability, allowing the potential entrance of toxins
into the brain. For compounds capable of this, such as glutamate, efflux mechanisms exist. Therefore, it is generally accepted that the BBB plays a crucial role in the determination of neurotoxicity and its prevention.1,2
There has been considerable progress made towards the understanding of the pathophysiology and mechanisms involved in blood-brain barrier permeability. In neurological disorders affecting the brain, the cerebral endothelium plays a crucial etiologic role when the BBB becomes disrupted or modified in a way that increases the vascular permeability.1 Various ways exist in which several molecules are able to pass the endothelium, including intercellular routes or direct transcellular penetration through a damaged endothelium. Dysfunction of the BBB may be caused by or a consequence of a particular disease process including but not limited to, neoplasia, ischemia, hypertension, dementia, epilepsy, infection, and trauma. It is questionable whether or not the BBB disturbance constitutes the main pathogenic factor that could elicit a sequence of events forming the final pathological state.1
