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article imageAutism's social deficits reversed with anti-cancer drug

By Tim Sandle     Mar 16, 2018 in Science
New York - New research suggests that autism's social deficits can be reversed by an established anti-cancer drug called romidepsin. This represents a breakthrough in epigenetics research.
The research, from the University at Buffalo, indicates that via an epigenetic mechanism, the drug romidepsin can restore gene expression and thus alleviate the social deficits in animal models of autism. Whether the same effect can be replicated on people will be the next phase of the research.
The study presents evidence that it may be possible to use a single drug compound to alleviate the behavioral symptoms associated with autism spectrum disorder. This is through using the drug to target sets of genes that appear to be associate with the disease.
Experiments have shown how a short-term treatment with an extremely low dose of romidepsin, which is an established anti-cancer drug, was able to restore social deficits in an animal models of autism. Romidepsin is an anticancer agent used in cutaneous T-cell lymphoma and other peripheral T-cell lymphomas. The drug product is a natural substance obtained from the bacterium Chromobacterium violaceum. The drug works in cancer treatment by blocking enzymes called histone deacetylases, which kills cancerous cells.
The three-day experiment succeeded in reversing social deficits in mice deficient in a gene termed Shank 3, which is an important risk factor for autism spectrum disorder. Specifically, mutations in this gene are associated with autism spectrum disorder. With the study, the positive effect lasted for three weeks.
Lead researcher Dr. hen Yan states: "We have discovered a small molecule compound that shows a profound and prolonged effect on autism-like social deficits without obvious side effects, while many currently used compounds for treating a variety of psychiatric diseases have failed to exhibit the therapeutic efficacy for this core symptom of autism."
The research has been published in the journal Nature Neuroscience and the paper is titled "Social deficits in Shank3-deficient mouse models of autism are rescued by histone deacetylase (HDAC) inhibition."
More about Autism, Learning, anticancer, Medication
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