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A protein that regulates the formation of myelin sheaths may lead to new treatments for multiple sclerosis.
A recent discovery that the development of new myelin sheaths is regulated by protein molecules may help treat patients with multiple sclerosis (MS) following a relapse.
In a study published in Nature Communications, a group of German scientists explored the mechanisms through which oligodendrocytes regulate the formation of new myelin sheaths. The research team previously identified protein molecules, such as Sox10, that manage the formation of new myelin sheaths and preserve existing ones.
Inhibiting Nfat proteins diminishes the capability of oligodendrocytes to form new myelin in humans, rats, and mice, according to the study. The researchers found even fewer Nfat proteins in oligodendrocytes in the parts of the brain that are affected by MS, but they are unsure whether this finding is linked to damage caused by the disease.
“The interrelationships are very complex,” study leader Dr Michael Wegner, chair of Biochemistry and Pathobiochemistry, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), said in a press release.
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Prior research into these mechanisms in patients with MS led to the use of treatments that hinder Nfat proteins, such as Cyclosporin A and Tacrolimus. These treatments are primarily used to regulate the immune system, such as in transplant patients to prevent organ rejection, according to the study.
However, the researchers noted that transplant patients sometimes experience neurological disorders resulting from the loss of myelin sheaths. They hypothesize that these adverse effects result from medications that inhibit Nfat proteins.
The findings of the study may hold significance to concurrent research at FAU that is exploring whether targeted stimulation of Nfat proteins could help spark the formation of new myelin sheaths in patients with MS following a relapse, the researchers concluded.
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