Families of children with mutations in a gene called SYNGAP1 have spurred research into the effects of the mutations on people — and how to treat them.

The signaling imbalance theory holds that the brains of autistic people are hyper-excitable because of either excess neuronal activity or weak brakes on that activity.

A huge new research collaboration may jump-start the race to develop therapies for autism.

Researchers have repurposed the gene-editing tool CRISPR to dial down a gene’s activity in select subtypes of neurons in mice.

A fusion of two existing drugs alleviates autism-like features in a mouse model of the condition.

The drug mavoglurant has no effect on a brain circuit involved in social behavior in a mouse model of fragile X syndrome. That may explain its poor performance in people with the condition.

Introducing the gene UBE3A into neurons that dampen brain activity prevents seizures in a mouse model of Angelman syndrome.

A gene called TRIO may be a hotbed for autism mutations, an international collaboration focuses on the whole brain and one behavior, and Autism Speaks cuts grant spending.

Music therapy proves ineffective for autism, brain structures differ with 16p11.2 duplications and deletions, and mice missing NLGN3 may influence the sociability of their littermates.