A protein known as Gsta4 is critical in the growth and activity of oligodendrocytes, a special type of brain cell that generates the myelin sheath that is damaged in multiple sclerosis (MS), a study shows.
The overproduction of Gsta4 in a MS rat model led to milder disease and lower disability scores compared to healthy rats. The authors suggest that Gsta4 may be an important therapeutic target for the development of reparative MS therapies.
The study, “Gsta4 controls apoptosis of differentiating adult oligodendrocytes during homeostasis and remyelination via the mitochondria-associated Fas-Casp8-Bid-axis,” was published in the journal Nature Communications.
MS is caused by the immune system attacking the myelin sheath, the protective coating that covers nerve fibers. Myelin is generated and maintained by cells called oligodendrocytes.
In the early stages of MS, oligodendrocytes mature from oligodendrocyte precursor cells (OPCs), creating new myelin (remyelination), which restores and maintains nerve cell function. However, over time, the formation of new oligodendrocytes is reduced along with the ability to remyelinate nerve fibers.
So far, the underlying mechanisms of this process remain unknown.
Now, researchers at the Karolinska Institutet in Sweden investigated these mechanisms to better understand the loss of oligodendrocytes.
“Too little is known about the mechanisms behind progressive MS, by which I mean the phase of the disease in which oligodendrocytes and neurons in the brain die without re-forming,” Karl Carlström, PhD, first author of the study, said in a press release.
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