A group of genetic variants that are linked to schizophrenia do not seem to be associated with autism, according to a study published in the January issue of the American Journal of Medical Genetics Part B.

Researchers have created a network of various forms of many proteins linked to autism, revealing new molecular interactions that may play a role in the disorder. The unpublished work was presented in a poster last week at the Salk Institute, Fondation IPSEN and Nature Symposium on Biological Complexity in La Jolla, California.

Rare, inherited mutations contribute to a significant proportion of autism cases, helping to explain the heritability of the disorder, according to two new studies published today in Neuron.

The genome appears to be littered with so-called ‘hotspots,’ areas that are prone to single-letter mutations, according to research published 21 December in Cell.

Members of families that have multiple children with autism have more features of the disorder than do those from families that have only one child with autism, according to a study published 2 November in the Journal of Autism and Developmental Disorders.

Most cases of Rett syndrome in China are the result of mutations on the paternal copy of MeCP2, according to a study published 27 August in the European Journal of Medical Genetics.

By merging genetic data from two large clinical repositories, from a total of more than 30,000 children, researchers have identified 18 copy number variants (CNVs) — DNA deletions or duplications — that play a role in autism. The findings appeared 9 October in Molecular Psychiatry.

A new candidate gene for autism, CHD8, may account for up to 0.4 percent of cases of the disorder, according to research published today in Science. CHD8 is one of six genes identified that together may contribute to one percent of autism cases.

The sperm of old mice has an unusual epigenome, the profile of chemical modifications to the underlying DNA code, according to a poster presented Saturday at the 2012 Society for Neuroscience annual meeting in New Orleans. The findings suggest an explanation for the so-called paternal age effect in autism.

Mutations in the CDKL5 gene lead to developmental delay starting at birth, seizures that begin before 3 months of age, and subtly atypical facial features, according to a study published 8 August in the European Journal of Human Genetics.