Some forms of autism are caused by too many proteins at the synapse, the junction between neurons, whereas other forms result from too few, according to a study published 23 November in Nature.

Three mutations in SHANK2, an autism-associated gene, each lead to abnormal synapses, the junctions between neurons, according to a study in Human Molecular Genetics.

Regions of the genome that contain the same genetic variants on both copies of a chromosome are more likely to contain autism-associated genes than other parts of the genome, according to a study published 14 October in Human Genetics.

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.

There are a host of problems with laboratory rodents that scientists rarely talk about, argues a fascinating series of articles in Slate magazine.

More than 70 percent of individuals lacking the autism-associated 16p11.2 chromosomal region are overweight or obese, according to a study published 20 September in the Journal of Genetics and Genomics.

Researchers have derived neurons from stem cells to investigate mutations that lead to Rett and fragile X syndromes.

In October, the autism science and advocacy organization Autism Speaks announced its plans to sequence whole genomes of 10,000 children with the disorder and their family members over the next two years.

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.