Clumsiness in children with autism may result from the same genetic mutations that contribute to the disorder, according to a study published in February in the Journal of Autism and Developmental Disorders.

Genetic syndromes associated with autism are increasingly being diagnosed in utero because of techniques that can identify subtle mutations in the genome. But the technology is ahead of the ethical debate on whether and how to inform parents about mutations with unknown effects.

Two children with Asperger syndrome have disruptions in the PARK2 gene — one child has a duplication in the gene whereas the other has a deletion — according to a study published in February in the American Journal of Medical Genetics.

A neurotransmitter called VIPR2, or vasoactive intestinal peptide receptor, is a candidate gene for schizophrenia and, potentially, autism, according to a study published in February in Nature.

An Italian group is investigating the provocative hypothesis that some cases of autism are the result of a viral infection passed from sperm to fetus.

In the world of Skype, instant messages and tweets, face-to-face interaction is still the best route to discovery, according to an intriguing study published in December.

A gene that regulates the conversion of testosterone to estrogen in the brain could help explain why males are more susceptible to autism than are females, according to a study published in PLoS One in February.

Neuroligin-4, a protein associated with autism, is located at synapses — the junctions between neurons — that inhibit signals in the brain, according to a study published in February in the Proceedings of the National Academy of Sciences. The protein can also single-handedly induce neurons derived from human stem cells to form synapses, according to another study in the same issue.

Disrupted-in-schizophrenia 1, or DISC1— a protein associated with both autism and schizophrenia — is involved in the transport of mitochondria, the power-houses of the cell, to their correct locations in neurons, according to a study published in February in Molecular Psychiatry.

Researchers have created a mouse carrying a deletion in SHANK3, an autism candidate gene, they reported yesterday in Nature. This is the second model of SHANK3 mutations but shows markedly more behavioral and brain defects compared with the first.