You’ll never hear Jacqueline Crawley talk about an ‘autistic mouse’. In fact, in her keynote address at IMFAR in May, she implored the audience to never use those two words in the same sentence.

If you believe the hype about oxytocin, it’s nothing short of a wonder drug: it can make you trust a stranger, enhance a mother’s bond with her child and, according to a study published earlier this year, improve social skills in individuals with autism. But look more closely, and there is ample cause for caution.

With robust training in developmental psychology and a techie’s fervor for new tools, Kevin Pelphrey is systematically investigating how the brain changes during development — starting in infants as young as 6 weeks old.

Families affected by fragile X syndrome can let out a modest cheer this week: the largest-ever randomized trial of a drug to treat the syndrome has just cleared its second phase.

Scientists have discovered that neurexins — proteins linked to autism — bind to a wide variety of molecules at the junction between neurons. In this complicated system, the breakdown of any one of the parts could lead to improper cell signaling, ultimately giving rise to disease.

Children with fragile X syndrome show abnormal growth in several brain structures during the first few years of life, according to the first study to track how the disease unfolds in the brain during early development.

Several independent groups have found previously unknown risk genes for autism, schizophrenia and mental retardation. The candidate genes have one thing in common: they encode proteins that are needed for the healthy function of synapses, the junctions between neurons.

A decade of research on the biology of autism, combined with a steady rise in diagnoses, has finally piqued the pharmaceutical industry’s interest in developing drugs for the disorder. Preliminary data from one small clinical trial already show positive results, and results from several others are expected early this summer.

A study of a rare form of epilepsy found in Amish groups adds heft to the idea that mTOR — a much-studied hub in a massive network of brain cell proteins — is an important biochemical player in autism.

FMRP, the protein missing in fragile X syndrome, is needed for the birth of new neurons, for regulating the translation of RNA into protein, and for maintaining the structural integrity of spiny neuronal projections, according to several new studies.