Altered electrical activity in the neurons of mice with a mutated copy of SCN2A may explain the animals’ autism-like social behaviors.

Thousands of protein-protein interactions mapped in mice reveal how these networks shift across seven kinds of tissue.

Brain responses to visual stimuli are smaller and weaker in children with Phelan-McDermid syndrome, an autism-linked genetic condition, than in non-autistic children.

Mice with autism- or schizophrenia-linked mutations only in the anterodorsal thalamus have problems with long-term and working memory.

Mounting evidence suggests that autism often involves upsets in homeostatic plasticity, a set of processes neurons use to stabilize their activity. These disruptions result from a range of autism-linked mutations and may help to explain the condition’s famed heterogeneity.

Brain cells from the cerebellums of mice that model tuberous sclerosis show dampened levels of proteins controlled by FMRP, the protein missing in fragile X syndrome.

Integrating genetic analyses into studies of babies’ brain development could help us understand how autism-related genes contribute to autism traits.

Biological factors that reflect autism’s roots may differ from those that influence how severe the condition is. Failure to make a distinction has stymied the search for biomarkers.

Problems with falling and staying asleep are common in autism, and they may be due in part to leaks in the blood-brain barrier, according to a new study in fruit flies.

A new technique can reveal where thousands of neurons send their axons — and measure the cells’ RNA levels for dozens of genes at the same time — in the mouse brain. It could be used to profile neural circuits underlying autism.