Several genetic and animal studies in the past year have found intriguing ties between autism and DISC1, one of the oldest candidate genes for psychiatric disorders.

Researchers are using dogs as models of psychiatric and behavioral conditions, including obsessive-compulsive disorder and autism.

Individuals who carry a large and rare deletion on chromosome 16 that is associated with autism are likely to have developmental delays, be obese or both, according to two studies published last week in Nature.

Autism may be the result of faulty wiring that occurs during early brain development, according to two independent studies that looked at the origins of circuit disruption.

Deletions or duplications of chromosomal segment 16p11.2 — previously reported as a key autism region — are seen in people with developmental delays and speech and behavioral problems, but not necessarily autism. That’s the finding from two large studies published last week of people carrying these rare genetic variations.

Variations linked to autism and schizophrenia crop up in people with a large variety of conditions, including bipolar disorder, seizures and obsessive-compulsive disorder, as well as in healthy people. This notion gained new support from unpublished data presented at the World Congress for Psychiatric Genetics in San Diego.

A common variant of a gene called CACNA1G — which makes a channel that helps regulate calcium flow between cells — may increase the risk of developing autism, according to research published in Molecular Psychiatry.

The molecular mechanisms underlying synaptic plasticity ― the ability of neurons to change the strength of their connections ― can vary across different inhibitory neural circuits as much as they can vary across excitatory neural circuits, according to research presented this morning at the Society for Neuroscience meeting.

Schizophrenia may be a consequence of neuronal birth gone awry, according to unpublished research presented today at the Society for Neuroscience conference.