Multiple sclerosis can have a devastating impact on people’s lives, affecting mobility, speech, mental ability and more
Multiple sclerosis affects around 2.5 million people around the world. Typically, people are diagnosed in their 20s and 30s, and it is more common in women than men. Although the cause has so far been a mystery, the disease causes the body’s own immune system to attack myelin – the fatty “sheaths” that protect nerves in the brain and spinal cord. This leads to brain damage, a reduction in blood supply and oxygen and the formation of lesions in the body. Symptoms can be wide-ranging, and can include muscle spasms, mobility problems, pain, fatigue, and problems with speech.
Scientists have long suspected that mitochondria, the energy-creating “powerhouse” of the cell, plays a link in causing multiple sclerosis. The 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.
Watch: Signs, symptoms and treatments for Multiple Sclerosis
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 published in the Journal of Neuroinflammation.