An international team involving the University of Exeter Medical School and the University of Alberta has discovered a new cellular mechanism – an underlying defect in brain cells – that may cause multiple sclerosis, and a potential hallmark that may be a target for future treatment of the disease.

Scientists have long suspected that mitochondria, the energy-creating "powerhouse" of the cell, plays a link in causing MS. The joint Exeter-Alberta research team was the first to combine clinical and laboratory experiments to explain how mitochondria becomes defective in people with MS. Using human brain tissue samples, they found that a protein called Rab32 is present in large quantities in the brains of people with MS, but is virtually absent in healthy brain cells.

Where Rab32 is present, the team discovered that a part of the cell that stores calcium (endoplasmic reticulum or ER) gets too close to the mitochondria. The resulting miscommunication with the calcium supply triggers the mitochondria to misbehave, ultimately causing toxicity for brain cells people with MS.

Researchers do not yet know what causes an unwelcome influx of Rab32 but they believe the defect could originate at the base of the ER organelle. The finding will enable scientists to search for effective treatments that target Rab32 and embark on determining whether there are other proteins that may pay a role in triggering MS.

The study was recently published in the Journal of Neuroinflammation.