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In the case of MS, it is nerve cells that get damaged, causing patients to experience increased disability over time. Treatments are available but there is no cure, and the exact cause of the disease remains a mystery.

Many scientists looking into MS have focused on a component within cells known as the mitochondria, which serves two purposes. The mitochondria is firstly a cell’s power plant — making energy to keep the cell alive — but it also acts a as a kind of “sentinel” that can trigger the cell to die if it becomes stressed by inflammation or some other factor.

In an effort to better understand how this happens, previous research by the U of A team and others has explored how the mitochondria interacts with another cell component called the endoplasmic reticulum — the part of the cell that stores calcium.

Simmen said some communication between the two components is required because this is how the mitochondria is told to make energy.

“But if the cell gets inflamed, then you get too much interaction, and all of a sudden the endoplasmic reticulum gets glued to the mitochondria and you get kind of a short circuit,” he said. “The calcium gets transferred over massively, the sentinel sounds the alarm and the cell commits suicide.”

Based on this finding, the U of A team decided to begin looking for molecules that might be kickstarting this harmful miscommunication. That led them to identify the protein Rab32, which is found in the brain samples of MS patients but is virtually absent in samples from healthy brains.