Inflammation at the blood–brain barrier in multiple sclerosis

Abstract

The blood–brain barrier is specialized to function as a barrier to protect the central nervous system (CNS) by restricting entry of unwanted molecules and immune cells into the brain and inversely, to prevent CNS-born agents from reaching the systemic circulation. The blood–brain barrier endothelium, together with the cells involved in its regulation, forms the neurovascular unit. Blood–brain barrier dysfunction is an important hallmark of early multiple sclerosis pathophysiology, leading to a consequent loss of the imperative brain homeostasis. The unrestrained access of immune cells and blood-borne compounds into the CNS play a central role in demyelination and axonal damage, two major hallmarks of multiple sclerosis pathology underlying the clinical symptoms of patients. The neuroinflammatory changes at the blood–brain barrier are numerous and include the loss of barrier function, altered communication with surrounding cells, and activation of both inflammation promoting and dampening mechanisms. A better understanding of the blood–brain barrier alterations in neuroinflammation might lead to new ways to promote blood–brain barrier function in neurological diseases like multiple sclerosis.