Unravelling a mystery cause of disease
A new study about Multiple Sclerosis Info has made a major new discovery towards finding the cause of multiple sclerosis (MS), potentially paving the way for research to investigate new treatments. 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 the disease, and a potential hallmark that may be a target for future treatment of the autoimmune disorder.
The study was recently published in the Journal of Neuroinflammation and part funded by the Royal Devon & Exeter NHS Foundation Trust.Professor Paul Eggleton, of the University of Exeter Medical School, give multiple sclerosis info that: “Multiple sclerosis can have a devastating impact on people’s lives, affecting mobility, speech, mental ability and more. So far, all medicine can offer is treatment and therapy for the symptoms — as we do not yet know the precise causes, research has been limited. Our exciting new findings and multiple sclerosis info 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 Multiple Sclerosis.”
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 joint Exeter-Alberta research and multiple sclerosis info team was the first to combine clinical and laboratory experiments to explain how mitochondria becomes defective in people with Multiple Sclerosis. 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 Multiple Sclerosis.