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.

A failed replication and other problems led autism researcher Beth Stevens and her co-investigator to retract the nearly 10-year-old report.

In mice with a mutated copy of SHANK3, stress induces social deficits and alters gene expression in certain excitatory neurons. But eliminating a stress-related protein that regulates SHANK3 restores typical social functioning in the animals.

Clues that problems with mitochondria contribute to autism have been accumulating for decades. In the past five years, a mutant mouse and a flurry of findings have energized the field.

The work fills in gaps about how synapses change before and after birth — essential knowledge for understanding whether synapse development differs in autism.

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.

A controversial idea about how cells compartmentalize their contents into droplets — like beads of oil in water — could be key to understanding autism, says Julie Forman-Kay.

Mutations in two genes linked to autism and intellectual disability boost the immune response and cause synapse dysfunction.

A novel microscopy technique offers the most detailed look to date at the proteins present at neuronal junctions.