MBD5, one of 20 genes located in the 2q23.1 chromosomal region, may be responsible for the autism-like syndrome caused by deletions in the region, according to a study published 7 October in the American Journal of Human Genetics.

A cancer drug shows promise as a treatment for Angelman syndrome, according to a study published today in Nature.

The brain abnormalities characteristic of tuberous sclerosis may begin early in development and involve malfunctioning of neuronal precursors, according to studies of two different mouse models of the disorder published in October.

The etiology of autism may be best understood as an impairment of neuronal circuits, specifically interneurons that dampen signals in the brain, says neuroscientist Gordon Fishell.  

Neurons from mice that model fragile X syndrome may fire signals more readily than neurons from controls, according to a study published 5 October in The Journal of Neuroscience. The results suggest a cause for the high incidence of seizures in individuals with the syndrome.

In high-functioning adults with autism, the signal-to-noise ratio in the outer regions of the brain is significantly lower than in healthy controls, according to unpublished research presented Friday in Washington, D.C.

Boys with autism have a distinct facial structure that differs from that of typically developing controls, according to a study published 14 October in Molecular Autism.

Teenagers with milder forms of autism withdraw socially in adolescence, even as some symptoms associated with the disorder wane.

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

Mice lacking the autism-linked gene CNTNAP2 show many of the behaviors associated with the disorder, and exhibit brain circuit disruptions similar to those seen in people who carry mutations in the gene.