Developmental delay, intellectual disability and behavioral issues are common among people who have mutations in MYT1L, a gene with strong ties to autism.

Treatments that counteract the effects of an SCN2A mutation in mice increase the animals’ sociability in adulthood, according to a new unpublished study.

The algorithm estimates a child’s likelihood of having autism from patterns of co-occurring conditions in electronic health records, outperforming a widely used screening test.

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.

Deleterious mutations in an autism-associated gene can make neurons hyperexcitable, raising the risk of epileptic seizures.

Activity patterns of neuronal networks link different genetic subtypes of autism that have similar traits, according to new unpublished research.