A team of researchers at Stanford Medicine has discovered that excessive activity in a specific brain region may underlie behaviors associated with autism spectrum disorder (ASD).

The study focused on the reticular thalamic nucleus, a structure that regulates the flow of sensory information between the thalamus and the cortex. Using a mouse model of autism, scientists found that this region displayed abnormal hyperactivity, which contributed to seizure susceptibility, sensory hypersensitivity, repetitive movements, hyperactivity, and reduced social engagement.

Remarkably, when the researchers suppressed this overactive brain region with drugs, the mice showed significant improvement, and many autism-like symptoms disappeared. These medications are already being evaluated for epilepsy, suggesting a possible shared mechanism between autism and seizure disorders.

The findings, published in Science Advances on August 20, were led by Dr. John Huguenard, professor of neurology, with Dr. Sung-Soo Jang, postdoctoral scholar, as first author.

The study further demonstrated that silencing this brain region through a genetic neuromodulation technique (DREADDs) also reversed behavioral symptoms, while artificially activating the region in healthy mice triggered autism-like traits.These results position the reticular thalamic nucleus as a promising target for future autism therapies.