Mice that lack the Rett gene in a subset of neurons that activate neural circuits develop tremor and anxiety-like behaviors, two characteristics of the syndrome.

These short reports from our reporter, Jessica Wright, give you the inside scoop on developments at the 2015 American Society of Human Genetics Annual Meeting.

Autism researchers are sharpening their statistical tools to make sense of the growing pool of autism genes.

Watch the complete replay of Huda Zoghbi discussing the genetics and molecular biology of Rett syndrome, an autism-like neurodevelopmental disorder.

Mice carrying any one of five autism-linked mutations struggle to associate a flash of light with an irritating puff of air. The findings suggest that the mice have trouble integrating information from multiple senses — a skill governed by the cerebellum.

A new study may help explain why the symptoms of Rett syndrome appear 6 to 18 months after birth. It suggests that the role of MeCP2, the protein missing in the syndrome, becomes more important as the brain matures.

Researchers from four labs were unable to reproduce the findings from a high-profile 2012 study in which bone marrow transplants dramatically extended the lives of mice with features of Rett syndrome. Their sobering findings were published yesterday in Nature.

The mutation that causes Rett syndrome may spark uncontrolled inflammation throughout the body and brain, suggests a study published last week. The findings may explain the syndrome’s wide range of symptoms, from seizures to gut problems.

Mutations in MeCP2, which cause Rett syndrome, boost the expression of long genes in the brain. The findings add to mounting evidence linking long genes to developmental disorders.

The little-studied autism gene ANKRD11 helps to package DNA in the nucleus and plays a critical role in the early growth and positioning of neurons.