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.

The language deficit in autism is complex and diverse. With a no-nonsense and thoughtful approach, Helen Tager-Flusberg has devoted her career to sorting it all out.

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

Toddlers with autism who have larger-than-normal heads are also taller and weigh more than controls, according to a study published in October in Archives of General Psychiatry.

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.

In families that have at least one child with autism, significant motor impairments crop up in most children with the disorder and hardly any of their unaffected siblings, according to a study published 19 October in Autism.