A University of Alberta researcher is set to demonstrate the potential of a brain molecule called fractalkine to halt and even reverse the effects of multiple sclerosis and other neurodegenerative diseases.
Multiple sclerosis is an autoimmune disease in which myelin, or the fatty lining of nerve cells, is eroded, leading to nerve damage and slowed signaling between the brain and body. Symptoms of MS range from blurred vision to complete paralysis, and although there are treatments, the causes are not fully understood and nothing exists to reverse the disease process. More than 90,000 Canadians live with MS, according to the MS Society.
In new research published in Stem Cell Reports, Anastassia Voronova, assistant professor and Canada Research Chair in Neural Stem Cell Biology, injected fractalkine into mice with chemically-induced MS.
She found that the treatment increased the number of new oligodendrocytes –; vital brain and spinal cord cells that produce myelin in embryonic and adult brains –; that are damaged during the autoimmune attack of MS.
If we can replace these lost or damaged oligodendrocytes, they could produce new myelin and it is thought that this would stop the progression of the disease, and even reverse some of the symptoms. It’s the holy grail in the research community and something we’re passionate about. »
Anastassia Voronova, Assistant Professor and Canada Research Chair in Neural Stem Cell Biology
Previous research by Voronova tested the safety and efficacy of fractalkine in normal mice and found similar beneficial effects. Other researchers have shown that fractalkine can protect nerves in mouse models before the disease is induced, but this is the first time it has been tested in animals that already have the disease.
Voronova and her team observed new oligodendrocytes, as well as reactivated progenitor cells capable of regenerating oligodendrocytes, in the brains of treated animals. Remyelination occurred in both white and gray matter. The researchers also observed a reduction in inflammation, part of the damage caused by the immune system. The next steps in the treatment are to test it in other diseased mouse models, including those with neurodegenerative diseases other than MS.