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.

The DNA specific to mitochondria is difficult to access, but new methods place its secrets within reach.

Of nine genetic models examined in a new study, all had some incidence of cardiac abnormalities. But the problems varied widely depending on the affected genes.

The findings, based on Swedish national registry data, suggest a critical need to expand mental health services for autistic people.

The gene, YTHDF2, may be one of several that contribute to an autism subtype marked by an unusually big brain.