Signaling imbalance, driven by too much excitatory activity, may be a consequence of whatever brain changes lead to autism rather than a cause of the condition.

Two studies find that connectivity patterns remain stable over time in people with ASD, while in typical subjects they change.

Contrary to prior evidence, a study finds receptor density is the same among people without and without the disorder, although GABA signaling still appears to be impaired.

After years of obscurity, strains of mice with mutations in particular genes are thrust to the fore of autism research.

Scientists are making use of Xenopus tadpoles to study autism risk genes. 

Patient-derived organoids reveal autism spectrum disorder–associated anomalies.

Replacing immune cells in a mouse model of Rett syndrome, a developmental brain disorder, improved symptoms, suggesting a new target for treatment.