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.

Mice lacking a copy of SHANK3, a gene associated with autism and intellectual disability, show marked improvements in brain signaling after being treated with insulin-like growth factor 1, according to unpublished findings presented Saturday at the International Congress of Human Genetics in Montreal, Canada.

Individuals who have autism and dysmorphology comprise a distinct subgroup within the disorder, says geneticist Judith Miles. 

Researchers have created detailed three-dimensional reconstructions of the numerous complex branches of dendrites, the signal-receiving ends of neurons.

Mice lacking a gene that regulates an important signaling pathway in the central nervous system have severe autism-like social deficits, including little interest in nurturing their offspring and problems with learning and memory.

Neurons in a mouse model of fragile X syndrome make more connections during a critical period in development compared with controls, but are slower to respond to signals.

Individuals with fragile X syndrome make slightly more eye contact in stressful social situations after taking oxytocin compared with placebo.

A variant of the FGF14 gene may decrease the volume of the amygdala, a brain structure needed to interpret emotions in facial expressions, according to results presented on Sunday at the World Congress of Psychiatric Genetics in Washington, D.C.

A new review suggests that sleep problems in neurodevelopmental disorders don’t just reflect underlying weaknesses in neural circuitry; they actively intensify these deficits.

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