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A genetic condition associated with autism undergoes significant brain connectivity changes during puberty, potentially explaining its link to psychiatric disorders, according to new research from University of California, Los Angeles Health and international collaborators.
Scientists found that chromosome 22q11.2 deletion syndrome – which is caused by missing genetic material on chromosome 22– produces dramatic shifts in brain connectivity patterns that coincide with puberty, according to findings published in Science Advances.
The research team used brain imaging in humans with the condition and laboratory mice with similar genetic modifications to track these changes.
“Differences in functional connectivity observed on MRI are commonly found in psychiatric disorders, but we don’t have a good understanding of why. It was really valuable to study this phenomenon across species,” said Carrie Bearden, professor at the UCLA Health Semel Institute and the UCLA Brain Research Institute.
Brain scans revealed that affected individuals show hyperconnectivity between brain regions before puberty, particularly in areas responsible for social functioning. After puberty, these same regions shifted to a pattern of under-connectivity compared to individuals without the genetic deletion.
Examining this pattern at the cellular level, researchers found that mice engineered with the genetic condition had more dendritic spines — which are structures the brain cell uses to form connections during early development. Following the equivalent of puberty in mice, these numbers declined sharply compared to mice without the genetic modification.
The research identified the protein GSK3-beta as playing a key role in regulating these connectivity changes. When researchers administered a GSK3-beta inhibitor to affected mice, they temporarily normalized both brain activity patterns and dendritic spine density.
Human brain imaging confirmed the regions showing connectivity changes had enriched expression of genes related to GSK3-beta. The connectivity alterations correlated with social behavior challenges in human participants.
“These findings strongly suggest that over-weeding of synapses during development may contribute to the behavioral challenges we see,” Bearden said.
The results indicate synaptic dysfunction may drive the observed changes in brain activity, pointing to potential targets for interventions that could address symptoms associated with the genetic condition.
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