The findings add to the growing evidence that genes with disparate functions can play similar roles in brain development.

UBE3A, a key gene associated with both autism-linked conditions, can explain most — but not all — of the syndromes’ atypical neuronal properties.

CRISPR-edited prairie voles that lack receptors for the so-called “social hormone” still bond with their mate and pups, raising questions about the molecule’s role.

The model enables the study of autism-linked genes at the earliest stages of neural development.

A young researcher faces down the skeptics.

The new tool may help researchers reconstruct the sequence of biological events that underlie development.

Strategies to replace or compensate for mutated copies of the TCF4 gene could lead to treatments for this profound form of autism, a new study suggests.

The DNA specific to mitochondria is difficult to access, but new methods place its secrets within reach.

A deactivated form of the gene editor restores UBE3A expression in mice and human neurons without cutting the genome. It may hold promise for future Angelman gene therapies.

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.