Long cast in supporting roles in the brain, astrocytes are now emerging as primary players in certain characteristics of autism and related conditions.

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.

The sex-specific effects may help elucidate why the small number of boys with DDX3X syndrome are born to unaffected mothers.

Ramping up levels of one isoform of the autism-linked protein reverses traits in model mice, a new study shows.

Interneurons that fail to propagate electrical signals in mice that model Dravet syndrome may cause the animals, like people with the autism-linked condition, to die suddenly.

Pups born to mothers that experience low oxygen during sleep have overactive mTOR signaling, which has been linked to some forms of autism.

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.

The protein, FMRP, shapes cell signaling near synapses but switches to regulate genes in the cell body, according to new research.

Mice missing a copy of the gene ASH1L have excess synapses and autism-like behavioral differences, some of which are reversed by boosting an ASH1L-regulated gene.