Researchers at the University of Geneva (UNIGE) have made a groundbreaking discovery in the field of autism spectrum disorder (ASD). By identifying a specific brain circuit responsible for social difficulties in people with autism, the study provides new insights into the neurobiological roots of these challenges, potentially leading to more targeted treatments. The findings, published in Molecular Psychiatry, reveal a defect in the communication pathway between two brain structures, hindering the ability to quickly shift attention—a crucial process for interpreting social cues.
Human survival and development are deeply reliant on social engagement, a skill that begins early in life. However, children with ASD typically show less interest in social stimuli from their first year, which impairs their ability to navigate the social world. To explore the origins of this phenomenon, UNIGE researchers combined clinical data with animal models to pinpoint the brain regions involved. Their discovery lays the foundation for predicting developmental outcomes and designing more effective interventions for those with ASD.
The Study and Its Methodology
Currently, it is estimated that one in every 36 children develops an autism spectrum disorder, with approximately one-third facing cognitive challenges. The research focused on understanding the brain’s role in ASD-related social difficulties, specifically how the brain redirects attention during social interactions. According to Camilla Bellone, Associate Professor in UNIGE’s Department of Basic Neurosciences, the lack of early social engagement in children with ASD impedes the development of essential social skills. “We learn through interaction with others,” Bellone explains, highlighting the importance of early social exposure in shaping a child’s cognitive development.
The study used mouse models to examine the brain networks involved in social behavior. The researchers studied mice lacking the Shank3 gene, a mutation commonly found in humans with ASD. These mice exhibit social orientation deficits that mirror the social difficulties observed in children with ASD, making them an ideal model for studying the disorder.
Findings from Mouse Models
The research team, led by Bellone and Marie Schaer, Associate Professor in Psychiatry at UNIGE, identified a critical communication pathway between two brain structures: the superior colliculus and the ventral tegmental area. The superior colliculus plays a key role in social orientation, while the ventral tegmental area is associated with the reward system. Bellone’s team discovered that a lack of neural synchronization in the superior colliculus disrupted communication between these two areas, impairing the mice’s ability to orient socially.
To monitor this brain activity in real-time, the researchers used miniaturized microscopes that allowed them to observe neuronal behavior in moving animals. This in vivo approach enabled them to capture the dynamic processes involved in the disruption of social behavior in the ASD model.
Translating Animal Findings to Humans
In collaboration with Marie Schaer’s team, Nada Kojovic, a researcher at UNIGE, developed an innovative protocol to obtain brain MRIs from young children with ASD, ages 2 to 5, without the need for sedation. “It is impossible to ask such young children to remain still in an MRI scanner for 30 minutes,” explains Kojovic. By developing a special habituation protocol and working closely with families, the team achieved high-quality MRI scans for over 90% of the children, despite their young age.
The team observed that the brain circuit identified in mice also existed in human children with ASD. Additionally, the degree of connectivity within this circuit allowed researchers to predict the children’s cognitive development over the following year. While direct interventions targeting this brain network are not yet feasible, the findings offer valuable guidance for behavioral therapies aimed at improving social attention in children with ASD.
Implications for Treatment
This discovery has significant implications for early intervention strategies. By reinforcing a child’s ability to quickly shift attention from one stimulus to another, targeted therapies could enhance social engagement from a young age. One such method, an intensive treatment used in both the U.S. and Geneva, involves 20 hours of therapy per week for two years. This treatment has already shown positive outcomes, and with the new insights from this study, future therapies may be better tailored to address the underlying neural mechanisms.
In conclusion, the identification of a specific brain circuit involved in social challenges in ASD provides a new perspective on the disorder’s neurobiological basis. This breakthrough offers hope for more precise interventions and a better understanding of how early social difficulties shape cognitive development in children with autism.
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