The finding that MDMA and an experimental serotonin agonist increase sociability across six different model mice suggests that disparate autism-linked mutations converge on the same underlying pathways.

Deleterious mutations in an autism-associated gene can make neurons hyperexcitable, raising the risk of epileptic seizures.

Spontaneous mutations in parts of the genome that regulate gene EBF3 appear to contribute to autism risk.

The software compares gene expression in cells derived from organoids with a reference atlas of the developing mouse brain.

A large, whole-genome sequencing study of families yields insights into ultra-rare genetic variants that contribute to autism.

Neurons in mice with an autism-linked mutation sprout extraneous protrusions, an overgrowth accompanied by above-average motor learning. Inhibiting a cell signaling pathway reverses the effect.

A transplant of inhibitory neurons during the second week of life prevents social difficulties and a brain signaling imbalance in mice missing a copy of FOXG1.

A mutation in the autism-linked gene SHANK3 changes how neurons encode information about social agency in mice.

Mosaic mutations, which affect only some of the body’s cells, play a small but meaningful role in autism. Though they are difficult to study, researchers are working to master their complexity.

Cross-species comparisons can help make sense of subtle genetic variants in people with autism and identify hundreds of new genes that may contribute to the condition.