A compound that shows promise as a treatment for fragile X syndrome alleviates repetitive behaviors in mice, but unexpectedly makes them less social.

Zebrafish share genes and pathways with humans, making them a useful tool to identify the genes that malfunction in autism, says expert Hazel Sive.

BTBR mice, which are less social than the typical B6 mice, have an elevated immune response in their brains and blood compared with those mice, according to a study published 20 July in PLoS ONE. Hybrids of BTBR and B6 mice have intermediate levels of immune molecules.

MeCP2, the protein missing in people with Rett syndrome, enhances learning and memory by binding to key genes and either activating or inhibiting their expression, according to a study published 17 July in Nature Neuroscience. Adding a phosphate to the protein in response to neuronal activity releases MeCP2 from these genes, the study found.

Researchers are creating a population of inbred lab mice with the potential to produce thousands of genetically diverse strains. Experiments using the first of these mice are published in the August issue of Genomic Research.

A new technique allows researchers to make stable modifications to neurons by incorporating modified amino acids into the proteins of stem cells. The method permits researchers to investigate neuronal function in live, intact cells.

Giving GLYX-13, a drug that targets an autism-associated brain pathway, to rats bred to be less social increases how much they communicate while playing.

The protein missing in people with fragile X syndrome regulates the activity of more than 800 other proteins, including some key players in autism, according to a study published 22 July in Cell. Many of these autism-associated proteins cluster on either side of the synapse, the junction between neurons.

Mice lacking SHANK1, a member of a family of autism-associated proteins, communicate less with their mothers and potential mates than controls do, according to a study published 9 June in PLoS One.

A multi-site collaborative venture between the U.S., Canada and Europe has created nearly 17,000 mouse embryonic stem cell lines, each lacking one of the genes in the mouse genome.