Misbehaving mitochondria may play MS role

May 03, 2017
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.

MS Focus Lending Library


Books, DVDs, and CDs are available for loan, by mail across the United States.
Learn more

Study uncovers potential risks of common MS treatment


Study finds an increased risk of events such as stroke, migraine, and depression, and abnormalities in the blood with taking beta interferon for MS.
Learn more

Environmental factors may trigger onset of MS

October 18, 2018

The findings may help explain the causes of MS and perhaps pave the way for a treatment or a cure.
Learn more