Researchers should proceed with caution when studying the behavior of one of the most popular mouse models of autism: the fragile X mouse model.

Deleting FMR1, the gene mutated in fragile X syndrome, in subsets of mouse neurons leads to distinct features of the condition.

Problems with social interactions stem from faulty wiring of a single circuit spanning distant brain regions, results from three mouse models of autism suggest.

A drug that has shown promise for treating fragile X syndrome may ease features of another condition associated with autism.

Differences in brain structure may distinguish boys with relatively mild features of fragile X syndrome from those with a severe form of the condition.

In people with fragile X syndrome, autism is often accompanied by seizures, trouble falling or staying asleep and anxiety.

A cannabis gel may ease features of fragile X syndrome, omega fatty acids show promise for autism in two trials, and oxytocin reinforces social behaviors through the brain’s reward pathway.

Some genes linked to autism regulate the production of proteins at neuronal junctions, suggesting that disrupted protein synthesis contributes to the condition.

Mice missing FMR1, the gene mutated in fragile X syndrome, have an atypical brain response to meeting an unfamiliar mouse.

People with autism aren’t easily surprised, the social camouflage some girls and women with autism use may preclude diagnosis, and autism-related genes are rooted deep in human ancestry.