The inflammation associated with the disease, particularly in mothers, may contribute to autism traits in children.

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

Siblings of autistic females are more likely to have autism than siblings of autistic males are, and mothers of autistic children carry more common, autism-linked variants than fathers do.

The gene helps neurons exit the cell-maturation cycle during fetal brain development, a new study shows. But male and female mice respond differently to DDX3X loss.

The approach, tested in mice, selectively boosts the expression of the autism-linked gene SCN1A in a subgroup of inhibitory cells.

The cells’ altered proliferation rates hint at ways to diagnose and potentially treat autism earlier.

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.

Different combinations of common, rare, inherited and spontaneous mutations may explain why traits vary so widely among autistic people.

Strategies to replace or compensate for mutated copies of the TCF4 gene could lead to treatments for this profound form of autism, a new study suggests.