A DLG2 deficiency in mice leads to reduced sociability and increased repetitive behavior accompanied by aberrant synaptic transmission in the dorsal striatum.

The study was conducted entirely in mice; findings do not directly translate to human clinical practice or therapy outcomes. The study used a global knockout of the Dlg2 gene, which does not model the specific genetic variations or partial deficiencies often seen in human patients. The researchers focused primarily on the dorsal striatum, so the role of other brain regions in these behavioral changes was not fully explored. The study establishes an association between synaptic changes and behavior but does not prove that the synaptic deficit causes the behavioral symptoms.

The paper notes support from the National Research Foundation of Korea (non-U.S. Gov't). No commercial conflicts of interest are declared in the provided text.

Do not interpret these findings as evidence for a treatment for autism. This is a basic science study describing brain mechanisms in mice. It does not test any intervention, and the behaviors observed in mice do not map directly to human social communication or repetitive behaviors in a way that changes clinical assessment or therapy.