Oxytocin therapies have failed to consistently benefit autistic people, but their effects in people with two autism-linked conditions may yield new insights, experts argue.

An overabundance of ribosomes drives an imbalance of proteins produced from long and short genetic transcripts in a mouse model of fragile X syndrome.

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

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

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 that express a fluorescent synaptic receptor reveal the interactions between neurons in unprecedented detail.

These short reports from Spectrum journalists highlight some of the autism-related findings that caught our attention at the meeting this past week.

Activating certain receptors in the amygdala — a treatment that runs counter to a leading theory of what causes the condition — can reverse some traits in rats.

Even partial loss of the gene impairs the mouse brain’s ability to respond to sensory experiences, which may explain why people with SYNGAP1 mutations tend to have learning difficulties and a high pain tolerance.