Scientists step closer to finding cause of multiple sclerosis

Written by Catharine Paddock PhD

As they find out more about the cell biology of multiple sclerosis , scientists are gradually unraveling the mysteries of the disease , although the exact causes are still unclear . Now , a new study continues this progress with a significant discovery about a new cellular mechanism . It suggests that high levels of the protein Rab 32 disrupt key communications involving mitochondria . The disruption causes these "cellular batteries " to misbehave , leading to the toxic effects seen in the brain cells of people with multiple sclerosis

The new study is the work of researchers from the University of Exeter in the United Kingdom and the University of Alberta in Canada. They report their findings in the Journal of Neuroinflammation.
Co-author Paul Eggleton, an immunologist and professor at the University of Exeter Medical School, says that multiple sclerosis can have a "devastating impact on people's lives," and yet, unfortunately, the present situation is that "all medicine can offer is treatment and therapy for the symptoms."
Multiple sclerosis (MS) is a disease in which the immune system mistakenly attacks tissue of the
central nervous system - which comprises the brain, spinal cord, and optic nerve.
As the disease progresses, it destroys more and more of the fatty myelin sheath that insulates and protects the nerve fibers that send electrical messages in the central nervous system.
This destruction can lead to brain damage, vision impairment, pain, altered sensation, extreme
fatigue , problems with movement, and other symptoms.
In earlier work, the team behind the new study was the first to provide an explanation for the role of defective mitochondria in MS through clinical and laboratory experiments.
In their new investigation, the researchers study a protein called Rab32, which is known to be involved in certain mitochondrial processes.
They found that levels of Rab32 are much higher in the brains of people with MS and hardly detectable in brains of people without the disease.
They also discovered that the presence of Rab32 coincides with disruption to a communication system that causes mitochondria to malfunction, causing toxic effects in the brain cells of people with MS.
The disruption is caused by a cell compartment called the endoplasmic reticulum (ER) being too close to the mitochondria.
The ER produces, processes , and transports many compounds that are used inside and outside the cell.
Study may lead to new MS treatments that target Rab 32
The researchers note that one of the functions of the ER is to store calcium, and if the distance between the ER and mitochondria is too short, it disrupts the communication between the mitochondria and the calcium supply.
Calcium uptake into mitochondria is already known to be critical to cell functioning.