Funding outcome

Multiple sclerosis (MS) is a disease affecting the brain and spinal cord, resulting in symptoms such as muscle weakness/spasms, fatigue and bladder problems. Underlying this are generalized changes in the nervous system, culminating in inflammation that results in the removal of myelin from nerve cells by blood cells. A type of white blood cell called a T-cell, becomes activated in MS patients and migrates from the blood across the blood brain barrier and attacks 'self-proteins', by secreting inflammatory chemicals that directly destroy the myelin sheaths surrounding nerve cells, or, signals other cells to attack the myelin proteins. Calnexin is an essential cell protein that helps produce many of the proteins that are released or retained on the surface of cells. The calnexin protein along with another protein called fatty acid binding protein 5 (FABP5) are highly abundant in MS patient's blood brain barrier cells. If either of these proteins is deleted it protects models of MS from developing MS-like disease symptoms. This suggests the amount of calnexin and FABP5 present may be important in controlling correct formation of myelin and function of the blood-brain barrier. We wish to study how removing calnexin/FABP5 complex protects against MS-like symptoms. This may lead to the identification of new therapeutic targets to address MS pathology.