A large scientific research company debuted seven new rat models of autism Tuesday evening in Washington, D.C. Two of the models, one lacking FMR1 and the other lacking NLGN3, show some unexpected new characteristics.

Postmortem brains from adults with autism have lower-than-normal levels of the fragile X mental retardation protein, which is missing in individuals with fragile X syndrome.

A compound that shows promise as a treatment for fragile X syndrome alleviates repetitive behaviors in mice, but unexpectedly makes them less social.

The protein missing in people with fragile X syndrome regulates the activity of more than 800 other proteins, including some key players in autism, according to a study published 22 July in Cell. Many of these autism-associated proteins cluster on either side of the synapse, the junction between neurons.

Small fragments of RNA, called microRNAs, can fine-tune the levels of proteins at the junctions between neurons in response to cell signals, according to a study published 10 June in Molecular Cell.

Blocking a chemical messenger — a much-touted approach to treating fragile X syndrome — is unlikely to completely reverse symptoms of the disorder, according to a provocative new study. The results, published in May in Behavioural Brain Research, show only modest behavioral improvements with the approach.

Several targeted trials on drugs that treat fragile X syndrome are under way. But accurate endpoints to measure the drugs’ effectiveness are crucial, argues developmental and behavioral pediatrician Randi Hagerman.

A new drug appears to relieve symptoms of fragile X syndrome by blocking the over-production of a key protein in a subset of people with the disorder, according to a 6 January study in Science Translational Medicine.

Treating adult mice with lithium restores the ability of neurons in fragile X mice to fine-tune their signaling, according to a study published online in November in Brain Research.

Inhibiting the ERK1/2 pathway — which regulates the synthesis of other proteins — can rescue some of the effects of fragile X syndrome, according to a study published 17 November in the Journal of Neuroscience. The ERK pathway could provide a novel target for fragile X therapies.