Fig. 10

Schematic diagram. Schematic representation of potential-triggered signals in RRMS patients responsible for the alteration in function and biochemistry of the ECs of the BBB. Pro-inflammatory mediators circulating in RRMS patients will affect the essential components of the BBB ECs named occludin, VE-cadherin as well as P-glycoprotein (P-gp). Adhesion molecules are also upregulated facilitating the adhesion and transmigration trough disruption of tight and adherens junctions. RRMS sera factor (pro-inflammatory and endocrine such as leptin) will also impact on the ECs metabolism down modulating the GLUT-1 receptor and triggering an impaired glucose (ECAR) and oxidative respiration (OCR) damaging the mitochondria and prompting the release of reactive species (ROS) which will further disrupt the neurovascular unit (basal lamina and astrocytes end-feet) targeting the neurons in the brain parenchyma