IBS team finds mechanism in autism impairs ability for social interaction

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A research team from the Institute for Basic Science (IBS) research team identified how autism spectrum disorders alter social interactions and provided clues to better understand and treat the decline in social communication caused by autism.

A research team from the Institute for Basic Science (IBS) has discovered how autism spectrum disorders alter social interactions and provided clues for a new way to treat the decline in social and cognitive function caused by autism.

In a previous study, the research team found that deleting the Shank2 protein causes dysfunction of the N-methyl-D-aspartate (NMDA) receptor, which plays a key role in synaptic and neuronal function, and can lead to autism. In a recent study, researchers revealed how problems at the synaptic level lead to social and cognitive decline.

Autism spectrum disorders are a type of developmental disorder of the brain affecting around 2% of the world’s population. Impaired social and cognitive skills are considered the main symptoms, but the exact mechanism has not been explained.

The research team, led by Director Kim Eun-joon of the IBS Center for Synaptic Brain Dysfunctions, put Shank2-suppressed autistic mice in contact with moving objects and other mice to find a link between changes in behavioral and cognitive functions of the brain.

In the brains of autistic mice, the NMDA receptor function of the neuron Parvalbumin (Pv), linked to the social and cognitive capacities of inhibitory neurons, was impaired. In addition, the decrease in the NMDA receptor lowered the triggering of the bursts to produce multiple electrical signals at once, inhibiting interactions between neurons.

The study showed that the NMDA receptor has problems and suppresses burst fire with the suppression of Shank2, resulting in impaired social and cognitive functions.

The researchers also found that this electrical synapse, a direct link between neurons, was over-enhanced in Pv neurons. A specific Pv neuron with optogenetic stimulation caused bursts of fire in neighboring Pv neurons through electrical synapses and restored social and cognitive abilities.

“We have been successful in improving social interaction by revealing a mechanism by which autism spectrum disorders induce a decrease in social skills, the main symptom of autism,” said Director Kim. “The results of the study will provide new direction for developing a treatment with a deeper understanding of autism.”

The research results have been published in the international online academic journal Nature Communications.


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