• Nicole Caropolo

Researchers Reverse ASD Symptoms In Mice

Mice have always been a staple in scientific studies. The reason behind mice being used for medical experiments is because they have similar behavior, genetic, and biological to humans. Drug testing, seizures, and Cancer studies have all used mice in the past as models. Recently, neuroscientists have used mice to analyze the gene that is missing from people with autism, which is called Shank3. They ended up making a discovery that could drastically change the future of people with ASD.

Using mice as models, researchers at MIT have been able to reverse the symptoms of autism by turning the gene later on. This results in a natural rewiring of the brain.

The Shank3 protein is what allows neurons to communicate in the synapses. Without it, autism symptoms surface such as compulsive behavior and avoiding social situations.

Guoping Feng, an MIT professor of brain and cognitive sciences, and his team genetically engineered mice to have their Shank3 turned off for embryonic development, but was later able to have it switched back on with the ingestion of tamoxifen. This resulted in the repetitive behavior exhibited by the mice to disappear, as well as an increase in social interaction.

This study allowed Feng and his fellow researchers to conclude that people with Shank3 mutations, especially those with ASD, could use the genome-editing process to fix the gene later on in the person’s life, resulting in an improvement of their symptoms.

General approaches for a larger population of people with ASD include identifying and modulating defective circuits for people with specific behavioral abnormalities

“This suggests that even in the adult brain we have profound plasticity to some degree,” said Feng. “There is more and more evidence showing that some of the defects are indeed reversible, giving hope that we can develop treatment for autistic patients in the future.”

For more information, visit MIT News and LiveScience.


©2020 ICare4Autism. All rights reserved.

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