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.

Early data suggest that it is possible to identify autism by looking at gene expression in the blood. But it’s going to take more work to prove it.

People with autism may belong to one of four distinct categories based on their medical history, according to a study published in the October Autism Research.

The Simons Simplex Collection (SSC), a database of genetic and clinical information from families that include one child with autism, has gathered data from more than 2,000 different families, researchers report in the October issue of Neuron.

Mice with social behavior deficits reminiscent of autism are friendlier when raised alongside a highly social mouse strain.

The first genome-wide linkage analysis of more than 1,200 families has identified regions implicated in autism as originating from either the paternal or maternal copies of chromosomes.

The National Institutes of Health on 30 September launched a public database to catalog a particularly important type of genomic data: so-called ‘structural variations’ — large deletions, duplications and rearrangements of DNA.

Researchers have mapped unique identifiers in the regions around human genes that are at risk for duplication or deletion, allowing precise sequencing of nearly 1,000 genes for the first time, according to a paper published today in Science.

A searchable new database will greatly ease the task of comparing results from more than 25 diagnostic tests for autism, by creating clusters of the various symptoms measured.

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.