Abstract: Neuroinflammation is a key process in the pathogenesis of various neurodegenerative diseases, such as multiple sclerosis (MS), Alzheimer ’s disease, and traumatic brain injury. Even for disorders historically unrelated to neuroinflammation, such as Alzheimer ’s disease, it is now shown to precede pathological protein aggregations. A common factor in these neurodegenerative diseases is activation of brain resident immune cells, as well as breakdown of the blood–brain barrier (BBB), which consecutively causes infiltration of peripheral immune cells, leading to neuronal damage and dysfunction. The integrity of the BBB, a biological barrier between the blood and the central nervous system, therefore plays a crucial role in regulating neuroinflammation. The BBB primarily consists of endothelial cells (ECs) that are tightly connected by tight junction proteins, astrocyte-end feet, and pericytes, conjunctively restricting the infiltration of immune cells and unnecessary biological molecules into the brain. BBB disruption, marked by the loss of structural integrity and upregulation of adhesion molecules and chemokines on the microvascular ECs, leads to infiltrating immune cells in the brain, driving neuroinflammation (Naegele and Martin, 2014).