Fragile X syndrome is a leading genetic cause of autism. People who have either condition often share certain traits, such as difficulties in social situations.

The protein missing in fragile X syndrome, FMRP, facilitates the production of hundreds of unusually large proteins, some of which are linked to autism.

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.