Scientists have pinpointed two major gene networks relevant to autism by analyzing gene expression in brain tissue from individuals with the disorder. Researchers presented the data Sunday at the Society for Neuroscience annual meeting in San Diego.

Researchers have developed the first stem cell system that makes it possible to study the early development of neurons from people with Rett syndrome, a rare disorder on the autism spectrum.

Blocking the expression of the MeCP2 gene decreases the number of synapses, the junctions between neurons. It also prevents synapses from scaling up their activity to make up for the loss, according to unpublished data shown yesterday at the Society for Neuroscience annual meeting in San Diego.

UBE3A, a protein mutated in Angelman syndrome and autism, regulates communication between neurons in the brain, according to a study published 29 October in Cell.

Researchers have narrowed down a genetic region associated with autism to one protein, cadherin 8, that helps bind cells together, according to a study published online in October in the Journal of Medical Genetics. This is the first time CDH8, the gene that encodes this protein, has been associated with autism.

Stem cell studies show that a mutation in the neuroligin-4 gene disrupts the normal development of synapses, the junction between neurons, according to unpublished data shown Sunday at the Society for Neuroscience annual meeting in San Diego.

A new mouse model for Rett syndrome shows that disrupting a single brain messenger can produce nearly all of the characteristic features of the syndrome, researchers report today in Nature.

An antipsychotic drug often prescribed to treat irritability in children with autism may be more helpful — and cause fewer side effects — depending on an individual’s genetic make-up.

Mice missing a large protein at the junction between neurons show motor impairments, anxiety and increased social behaviors, according to a study in the American Journal of Psychiatry. The protein, postsynaptic density-95 or PSD-95, is part of a key molecular bridge connecting other proteins linked to autism.

SHANK1 — a member of a family of proteins linked to autism — does not cause autism-like social deficits when mutated in mice, according to a study published online in September in Brain Research.