Mice exposed to unusually low levels of the placental hormone allopregnanolone in the womb show atypical brain development and autism-like behaviors.

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

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.

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.

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

A mouse model hints that genes linked to inflammation in some women may increase the likelihood of autism in their children.

Over the course of a career spanning more than three decades, Huda Zoghbi has won almost every major biology and neuroscience research award that exists. More than 20 years since she discovered the gene behind Rett syndrome, she remains laser focused on unlocking the condition’s secrets and finding effective treatments.

Mutations in CUL3, a leading autism gene, may disrupt the movements of neurons during development; correcting this misdirection could lead to an autism therapy.