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Repairing MS Nerve Damage With Cashew Shell Compound

Repairing MS Nerve Damage With Cashew Shell Compound
Credit: LoggaWiggler from Pixabay

Scientists from Vanderbilt University have discovered that a chemical compound from cashew nuts could unlock new treatments for autoimmune diseases such as MS (multiple sclerosis). Anacardic acid, which is found in the shell of cashew nuts, appeared to repair nerve damage and other symptoms of MS, in lab tests on rats and cell cultures.

Patients who are diagnosed with MS will see their immune system mistakenly attacking the insulating layer around nerves known as myelin. As myelin is slowly eaten away, it becomes difficult for signals to get through, resulting in issues with muscles, coordination, and vision.

The research, published in Proceedings of the National Academy of Sciences, found that anacardic acid triggers a chain reaction that promotes the repair of myelin, which could lead to slowing or even reversing this demyelination process.

In previous studies, the team found that a protein called interleukin 33 (IL-33) helps myelin form. They also identified an enzyme called histone acetyltransferase (HAT) that’s linked to IL-33, and when HAT was inhibited, the production of IL-33 increased, which could, in turn, help repair myelin.

Since anacardic acid is a HAT inhibitor, the team conducted several trials on rats and cultured cells to verify if the compound could be used as a potential treatment for MS.

Repairing MS Nerve Damage With Cashew Shell Compound
An artist’s illustration of a healthy nerve (left) with intact myelin, compared to damaged myelin like that in MS. Credit: lightsource/Depositphotos

One of the experiments involved the researchers culturing a rat cell called oligodendrocyte precursor cells (OPCs), which play a significant role in myelination. When anacardic acid was added, the expression of myelin genes and proteins increased, along with the production of IL-33. Levels of myelin basic protein also amplified as the dose increased.

Other experiments on rats with demyelination, showed that anacardic acid increased the number of OPCs that expressed IL-33, and lowered the physical effects of paralysis. The rats were dissected after death, showing an increase in myelination in line with the various doses they received.

These studies are in their beginning stages, and there’s no guarantee that the results will make their way to humans. However, the findings suggest that further research and trials should be conducted to explore anacardic acid for these kinds of demyelinating illnesses.