Researchers at the Institute of Basic Science (IBS) have identified a neural circuit in the brain linked to social impairments caused by autism spectrum disorder (ASD).

An IBS research team, led by Professor Kim Eun-joon, has identified neural circuit linked to social impairments caused by autism spectrum disorder.
An IBS research team, led by Professor Kim Eun-joon, has identified neural circuit linked to social impairments caused by autism spectrum disorder.

ASD is characterized by reduced sociability and repetitive behaviors, affecting approximately 2.8 percent of the global population.

Despite its rapidly growing prevalence, the exact cause of the disorder remains elusive, with no approved treatments yet available, and the correlation between ASD and brain neural circuits, which are responsible for controlling brain functions, was largely unknown.

In previous studies, the team, led by Professor Kim Eun-joon of the Synapse Brain Disease Research Center, reported that neurons in the prefrontal lobe of the cerebrum are overactive in a mouse model of autism that lacks the synaptic protein IRSp53, leading to reduced socialization in patients with autism.

The team's most recent study found that overactive prefrontal neurons in the brain impair reward circuits in the hypothalamus and midbrain, leading to reduced socialization in people with autism.

"One of these brain circuits, the reward circuit, plays a pivotal role in reinforcing essential survival behaviors," the team said. "In social animals like mice and humans, the reward circuit amplifies sociability by inducing positive emotions through the secretion of the neurotransmitter dopamine when they engage in social interactions."

However, in the autism mouse models, hyperactive neurons in the cerebral prefrontal cortex were found to abnormally suppress these reward circuits, leading to reduced social tendencies, it added.

The team stressed that the brain's ventral tegmental area, which intensifies sociability by releasing dopamine during social interactions, was abnormally inhibited in autistic mouse models.

The team also provided a clue to possibly curing such symptoms as it successfully normalized the reward circuit by using light stimulation on the hypothalamus neurons.

This led to the normalization of dopamine-producing neurons and resulted in the restoration of sociability in the autism mouse model, confirming the link between hyperactivity in the cerebral prefrontal cortex and reduced social tendencies due to the suppression of the reward circuit.

"This study in mice models of autism has identified neural circuits involved in the regulation of social behavior in autism," Professor Kim said. "Further studies will identify additional brain regions and neural circuits that may be associated with autism spectrum disorders, which could be used to understand and treat the cause of autism."

The study results were published in the online edition of Molecular Psychiatry last Wednesday.

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