These protective effects were associated with maturation of myelin-producing cells and production of IL-33, an immune-related molecule with a neuroreparative role in the central nervous system (CNS, the brain and spinal cord).
These findings suggest that treatment with anacardic acid may be a new potential therapeutic approach for demyelinating diseases such as MS.
“We see this as an exciting finding, suggesting a new avenue in the search for therapies to correct the ravages of MS and other demyelinating diseases,” Subramaniam Sriram, MD, the study’s senior author, said in a Vanderbilt University Medical Center (VUMC) press release. Sriram is VUMC’s chief of neuroimmunology and the William C. Weaver III professor of neurology.
The study, “Anacardic acid induces IL-33 and promotes remyelination in CNS,” was published in the journal PNAS.
In the brain, damage of myelin (the protective sheath around nerve fibers that is lost in MS) attracts immature, stem-like cells called oligodendrocyte precursor cells (OPCs) to the lesion site. These OPCs then mature into oligodendrocytes, which are myelin-producing cells capable of restoring the myelin sheath.
However, despite the presence of these progenitor cells in MS lesions, remyelination, or myelin repair, is incomplete or absent. Therefore, increasing efforts are focused on identifying potential therapeutic approaches to promote oligodendrocyte maturation and/or remyelination.
IL-33 is an immune signaling molecule found at high levels in the CNS — particularly in oligodendrocytes — where it has immunoprotective and neuroreparative properties. It was shown to promote remyelination after CNS injury in mice and reduced disease severity in a mouse model of MS.
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