Ahead of MS Awareness Week, which starts today, researchers unveiled a new cellular mechanism - an underlying defect in brain cells - that may cause the disease, and a potential hallmark that may be a target for future treatment of the autoimmune disorder.
"Multiple sclerosis can have a devastating impact on people's lives, affecting mobility, speech, mental ability and more," said Professor Paul Eggleton, of the University of Exeter in the UK.
"Our exciting new findings have uncovered a new avenue for researchers to explore. It is a critical step, and in time, we hope it might lead to effective new treatments for MS," he said.
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.
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.
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.
Disclaimer: No Business Standard Journalist was involved in creation of this content
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