A protective pathway that pauses protein synthesis is muted in a mouse model of fragile X syndrome, according to a new study.

The findings in rhesus macaque monkeys may provide clues to sex differences in the heredity of social behavior in people.

Over one hour, a particularly motivated mouse poked its nose 350 times into a hole in the test chamber in the hopes of meeting a playmate.

The newfound DNA-cutting enzyme, called Fanzor, can be programmed to edit the human genome and could prove easier to deliver to cells than current CRISPR tools.

Knocking down the gene that codes for the proteins normalizes the vocalizations.

The mutation increases the activity of an autism-linked protein and leads to social difficulties and other behavioral differences in mice.

The inhibitory cells misfire and contribute to social difficulties in mice that model the syndrome.

The variants are associated with slight differences in measures of intelligence, income and employment, but the relationship may not be causal.

Contrary to conventional wisdom, most people with fragile X syndrome express the FMR1 gene — albeit improperly.

The discovery could help clinicians diagnose children who carry mutations in the gene, called SCN2A, and gauge their responses to potential therapies.