Long-term treatment with antipsychotic drugs and mood stabilizers can change the structure of the brain.

The past few years have seen an unprecedented number of clinical trials for experimental drugs to treat autism-related disorders, most notably for fragile X syndrome. But as the trials progress, scientists are calling for better methods to measure the drugs’ effectiveness.

Clinical trials for fragile X drugs should include a behavioral therapy component, says a parent of a child with the disorder.

A promising approach to treating fragile X syndrome could benefit people even after the critical window of early brain development, and alleviate core symptoms of autism, according to two studies published this month.

In the last three years, autism researchers have gone from sequencing single genes to whole exomes, as highlighted at the Translational Neuroscience Symposium in Switzerland last week.

Children with autism carry twice as many new and damaging genetic mutations as typically developing children, according to a new study published in Neuron. The researchers also identified intriguing genetic links between autism and fragile X syndrome.

Mutant mice with autism-like behaviors have fewer behavioral impairments when provided with toys, exercise wheels and contact with other mice, than do those that live in typical laboratory cages, according to a study published 5 April in Human Molecular Genetics. 

Researchers have generated neurons from the blood cells of individuals with autism, according to a study published 7 March in Neuroscience Letters.

Dysregulation of the intracellular signaling pathway RAS, a risk factor for idiopathic autism, may provide a unifying theory of the disorder. Although this is not an altogether new hypothesis, several new findings have strengthened the evidence for it considerably.

The characteristics, interactions and roles of autism-associated genes in the fruit flies’ brain will help guide how we think about the same genes in humans, says Ralph Greenspan.