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

The postmortem brain tissue available for autism research is overwhelmingly from people of Western European heritage. Verónica Martínez-Cerdeño and her colleagues are working to change that.

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.

The possibility of microbial treatments for autism has inspired a burst of research and nascent clinical trials, but new research suggests these efforts rest on shaky scientific ground.

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.

The first animal model of MYT1L syndrome suggests that fast-maturing neurons lead to the unusually small brains, social deficits and other traits seen in people with the condition.

A new resource profiles gene expression and the accessibility of DNA in single cells across the developing human cerebral cortex and may help scientists decipher the effects of noncoding mutations linked to autism.

Autistic people have a higher-than-average chance of developing a neurodegenerative condition, according to a few studies. Some scientists are searching for proof — work that could also improve care for older autistic adults.