Cashew Shell Compound Has the Ability to Mend Damaged Nerves

Cashew shell compound has the ability to increase myelin. Demylination is key in multiple scelorsis and other diseases of the central nervous system.

Cashew nuts contain a chemical compound in the shell that can repair myelin, according to a new study by a team from Vanderbilt University Medical Center.

The study is published in the Proceedings of the National Academy of Sciences.

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‘Anacardic acid present in cashew nut shell can induce myelin formation by producing interleukin-33. Potential in treating demylinating diseases including multiple sceloris.’
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Myelin is a protective sheath surrounding nerves. Damage to this covering -- demyelination -- is a hallmark of multiple sclerosis and related diseases of the central nervous system.

"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," said the paper's senior author, Subramaniam Sriram, MBBS, William C. Weaver III Professor of Neurology and chief of the Division of Neuroimmunology.

Previous work led by Sriram showed that a protein called interleukin 33, or IL-33, induced myelin formation. IL-33 is, among other things, an immune response regulator, and multiple sclerosis is an autoimmune disorder.

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The cashew shell compound is called anacardic acid. Sriram and team grew interested in it because it's known to inhibit an enzyme involved in gene expression called histone acetyltransferase, or HAT, and the team had discovered that whatever inhibits HAT induces production of IL-33.

The report includes a range of new findings that point to potential therapeutic use of anacardic acid for demyelinating diseases:

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In vitro, the addition of the compound to rat cells most responsible for myelination -- oligodendrocyte precursor cells, or OPCs -- spurred induction of IL-33 and rapidly increased the expression of myelin genes and proteins, including dose-dependent increases in myelin basic protein
In two animal models of demyelination, treatment with the compound increased the relative presence of IL-33-expressing OPCs and led to reduced paralysis
In an animal model of demyelination treated with the compound, dissection and electron microscopy showed dose-dependent increases in myelination

"These are striking results that clearly urge further study of anarcardic acid for demyelinating diseases," Sriram said.

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Source-Eurekalert