Scientists May Have Discovered New Avenue Of Treating Multiple Sclerosis Patients

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U of A scientists found a new cellular mechanism in the fight against multiple sclerosis (MS), an underlying defect in brain cells that may a cause of the disease, and a potential indication that may be a new focus for future treatment. Fabrizio Giuliani, study co-author, U of A neurologist and medical director of the Northern Alberta MS Clinic, said the discovery opens the door to a brand new area of study in the battle against the cryptic autoimmune disorder that strikes more Canadians than any other nationality globally.

Thomas Simmen, study co-author and cell biology professor stated, “Scientists have been pointing to the mitochondria, the powerhouse of the cell, as a possible link to MS, but have not been able to decipher how they malfunction. Ours is the first study that combines clinical and lab experiments to explain how mitochondria become defective in MS patients.” Using human brain tissue samples, the scientists found how two sub-components within a cell are having a miscommunication in MS patients, and identified how at least one protein (Rab32) is causing the dysfunction.

Simmen stated, “A part of the cell that stores calcium (ER or endoplasmic reticulum) gets too close to the part of the cell that creates energy (mitochondria) when massive amounts of Rab32 are present in the brain of MS patients. The resulting miscommunication with the calcium supply triggers the mitochondria to misbehave, ultimately causing toxicity for brain cells in MS patients.”

Simmen added that In healthy brain tissue samples there is virtually no Rab32 present. Scientists do not know why or what causes an unwelcome influx of Rab32 but they believe the defect could derive at the base of the ER. Simmen continued, with this finding in hand, not only can researchers look for effective treatments that target Rab32, they can embark on determining whether there are other proteins that may be at play. He said, “Rab32 is just one of the proteins that is having the effect of drawing the ER and mitochondria too close. There are dozens of other possibilities.”

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