Research moves closer to unravelling mystery cause of multiple sclerosis

April 24, 2017
Demyelination by MS. The CD68 colored tissue shows several macrophages in the area of the lesion. Original scale 1:100. Credit: Marvin 101/Wikipedia

A new study has made a major new discovery towards finding the cause of multiple sclerosis (MS), potentially paving the way for research to investigate new treatments.

Ahead of MS Awareness Week, which starts today (Monday April 24), 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 —that may cause the disease, and a potential hallmark that may be a target for future 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, said: "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 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."

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 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, play a link in causing .

The joint Exeter-Alberta research team was the first to combine clinical and laboratory experiments to explain how mitochondria become 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.

Dr David Schley, Research Communications Manager at the MS Society, said:

"No one knows for sure why people develop MS and we welcome any research that increases our understanding of how to stop it. There are currently no treatments available for many of the more than 100,000 people in the UK who live with this challenging and unpredictable condition. We want people with MS to have a range of treatments to choose from, and be able to get the right treatment at the right time."

Explore further: Possible new target for treatment of multiple sclerosis found

More information: Yohannes Haile et al, Rab32 connects ER stress to mitochondrial defects in multiple sclerosis, Journal of Neuroinflammation (2017). DOI: 10.1186/s12974-016-0788-z

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Porgie
1 / 5 (2) Apr 24, 2017
Its the same one that causes liberals. Ahhhhhhhhhh But seriously folks we need progress on this. Thanks for your hard work.
BubbaNicholson
1 / 5 (1) Apr 24, 2017
Since the autoimmune diseases kill people, and since populations in the wild all control their populations with pheromones, usually at nesting sites ("displacement activity" and "nuptial dances" are necessary pheromone recognition behavior readying thin layer chromatographic surfaces behind the nostrils by covering it with lacrimal fluid containing dissolved pheromone receptor proteins)--or other pre-reproductive grouping, whether predisposing to predation or mating denial, it is logical that human autoimmune diseases are pheromonal, given that they accomplish exactly the same result: population limitation.
Since pheromones, like hormones, can be oppositional--one canceling the other--it is logical that oppositional pheromones might alleviate symptoms of MS and other autoimmune illnesses. A candidate is healthy adult male facial skin surface lipid pheromone usually exchanged in kissing, about 250mg by mouth is fairly well tolerated. Use extreme caution handling the pheromone.
BubbaNicholson
1 / 5 (1) Apr 24, 2017
When collecting, handling, packaging, and administering paternal facial skin surface pheromone, staff to wear supplied air respirators with full face shields. Make sure the atmosphere is turbulent by placing oscillating fans around the work area to break up plumes. Use fume hoods to store pheromone. Package the pheromone in sealed containers with activated charcoal dunnage. The undetectable odor of the pheromone at the ultra-trace level (ppb) has deleterious behavioral effects: astonishment/stupidity, superstition, suspicion, arrogance, and jealousy. Osculation partners of people treated by skin surface pheromone taken by mouth, always become artificially jealous. Artificial jealousy is felt just as severely as the real thing, and oddly, there is no way to dissuade even the smartest people from their superstitions, suspicions, and/or jealousies. Virtually every human pheromone discovery team has broken up quarreling because they failed to take proper precautions.
BubbaNicholson
1 / 5 (1) Apr 24, 2017
Pheromone recognition is insidious, so there is no self-recording of pheromone recognition results, plus the skin surface pheromone is itself without taste, color, or recognizable odor. The best way to tell that you have a leak is when your administering nurse turns around and slaps your face in front of the patients.
Use ordinary, fresh, new, un-chewed sticks of ordinary Wrigley's chewing gum to both collect and administer the skin surface pheromone. Illuminate the pheromone collected on the surface of the gum with UV at germicidal wavelength to reduce chance of disease transmission. Administer the dose (250mg) at one time; this involves chewing up to 15 pieces of pheromone laced gum in one sitting. Observe the dosing closely but unobtrusively as some autoimmune illnesses, like anorexia nervosa, produce mischievous behavior. A hidden camera is a wise precaution.
BubbaNicholson
1 / 5 (1) Apr 25, 2017
Myelination is dependent upon pheromones in the murine model. Maternal feces contain the pheromone and are consumed by offspring. Failure to consume the maternal feces results in less myelination in mice. Obviously we do not consume maternal feces, we get our pheromone from kisses, mostly.

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