The ability to conduct large-scale screening in human neurons could accelerate the discovery of autism treatments.

The investigational drug arbaclofen makes autistic people’s brains respond to a visual task more like non-autistic people’s brains do.

Mice missing the autism-linked gene SHANK3 use more neurons to engage in social behavior than control mice do, reflecting a more disorganized, less efficient brain signaling network.

The investigational drug arbaclofen may right an imbalance between inhibitory and excitatory signaling in the animals’ brains.

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.

Looking at the brain as a whole suggests that nudging flawed sets of neurons to collaborate better might alleviate autism traits.

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.