Lamotrigine Drug Can Reverse Autism-linked Behaviors in Mice, Study Finds; Hints at Cure for ASD

A new study found that the drug lamotrigine, used to treat epilepsy and stabilize mood in people with bipolar disorder, worked to stop behaviors like hyperactivity that are linked to autism in mice, SciTechDaily reports.

Scientists from the Hector Institute for Translational Brain Research carried out the research. They found that the functional changes and symptoms of autism are caused by a transcription factor called MYT1L that usually protects the molecular identity of nerve cells.

In mice, the drug lamotrigine was able to reverse the effects of MYT1L failure and fix the problems with how the mice worked and behaved. The study's promising findings boost optimism for developing an autism cure.

Autism Spectrum Disorders

Autism spectrum disorders (ASD) are complex developmental disorders characterized by impairments in social, communication, interest formation, stereotypical behavior patterns, epilepsy, or hyperactivity.

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Autism has been related to genetic factors, and scientists are trying to identify molecular abnormalities contributing to the illness.

Autism Treatment

Available treatments for autism spectrum disorder (ASD) aim to lessen symptoms that affect everyday life and quality of life, according to the CDC. As ASD has varied effects on different people, treatment plans typically involve several specialists and are personalized for each patient.

Meanwhile, there are still no drugs that can treat the core symptoms of ASD.

Autism Cure Study

The transcription factor MYT1L decides which genes in a cell are active and which are not. Almost all nerve cells in the body make MYT1L for their whole span. MYT1L keeps nerve cells from becoming muscle or connective tissue by blocking other developmental pathways that tell a cell to become muscle or connective tissue.

In a recent study, scientists genetically turned off MYT1L in mouse and human nerve cells. They found that this led to electrophysiological hyperactivation in mouse and human neurons, which worsened nerve function. Mice that did not have MYT1L had brain abnormalities and acted in ways that are distinctive of autism, like being less social or hyperactive.

The neurons missing MYT1L made too many sodium channels, typically only found in heart muscle cells. Sodium channels let sodium ions pass through the cell membrane, which is vital for electrical conductivity and how cells work.

In MYT1L-deficient nerve cells, the drug lamotrigine, which is used to stop seizures, was able to improve the function of brain cells and block autism-like changes in behavior. In mice, the drug could even stop symptoms like hyperactivity that are common in people with autism.

More Clinical Trials in the Future

The study only looked at the effects in mice, and there have been no clinical trials with people who have autism spectrum disorder.

However, the findings suggest that drug treatment in adulthood can alleviate brain cell dysfunction and reverse the behavioral abnormalities typical of autism. Clinical studies involving people with autism spectrum disorders are only getting off the ground.

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