Many people with fragile X syndrome show average rates of protein production, challenging a long-held assumption about the condition.

The drug mavoglurant has no effect on a brain circuit involved in social behavior in a mouse model of fragile X syndrome. That may explain its poor performance in people with the condition.

Researchers have used transcranial magnetic stimulation to show that people with fragile X syndrome have weak ‘inhibitory’ signals, those that dampen neuronal activity in the brain.

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.

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

Conventional wisdom holds that people with autism don’t get hooked on alcohol or other drugs, but new evidence suggests otherwise.

Clinical trials for autism drugs have been plagued with problems: bad design, the wrong measures, too broad a range of participants. All that is finally starting to change.

Our infographic displays efforts to develop treatments for fragile X syndrome. So far, none of them have passed muster in clinical trials.

A new genetic trick allows researchers to quickly spot the most promising treatments for fragile X syndrome among thousands of candidate compounds.