Deleting a copy of the gene TBX1 depletes the fatty myelin insulation that surrounds neurons and reduces cognitive speed in mice.

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

Dysfunctional circuits and a rogue sodium channel in the brainstem may explain the disordered breathing pattern seen in children with Pitt-Hopkins syndrome, a form of autism.

Audrey Brumback riffs about volunteering in Mexico, having a lab next door to her husband’s and why she sometimes cries at work.

Social memory, which may be altered in autism, depends on serotonin-sensitive neurons that send signals from the medial septum to the hippocampus.

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.

Jolting a bundle of nerve fibers deep in the brain restores learning and memory in mice with mutations of the autism-linked gene CDKL5.

The new technique can record hundreds of thousands of neurons firing nearly simultaneously across big swaths of brain tissue in living mice.

Scientists should heed these differences when considering resting-state brain activity as a biomarker for autism, the researchers say.

Ethan Scott packs his lab with math, physics and computer science experts to decode sensory brain networks in zebrafish models of autism.