Therapies that target the circuit could boost social activity, new findings suggest.

ADNP and SHANK3 proteins may bind together and alter a neuron’s internal scaffold, hinting at a mechanism that, when disrupted, may underlie several forms of autism.

Neurons with a faulty copy of SETD1A, a gene tied to autism and schizophrenia, show structural abnormalities and altered connectivity patterns.

Having a genetic predisposition to inflammation is linked to structural changes in brain regions implicated in neurodevelopmental conditions.

Sleep problems may contribute to or derive from autism traits — or both. After decades of work, researchers are beginning to uncover the biological connections between the two conditions, revealing new paths to potential treatments.

Some copy number variants may boost a person’s chances of having autism, but to a lesser extent than previously thought.

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.

Children born to mothers who take antipsychotic drugs during pregnancy are not more likely to have autism or attention deficit hyperactivity disorder, or to be born preterm or underweight.

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

Many genes linked to autism, schizophrenia and neurodevelopmental delay regulate gene expression and support communication between neurons.