Mice lacking a gene that regulates an important signaling pathway in the central nervous system have severe autism-like social deficits, including little interest in nurturing their offspring and problems with learning and memory.

Methylation marks were thought to be permanent features of the genome, but a new study challenges that idea.

The more we find out about human genetics, the more valuable model organisms are likely to become, say autism researchers.  

Neurons in a mouse model of fragile X syndrome make more connections during a critical period in development compared with controls, but are slower to respond to signals.

Probiotic bacteria alleviate stress in healthy mice and modify the expression of receptors for a chemical messenger that inhibits signaling in the brain.

Loss of MeCP2, the Rett syndrome gene, in neurons that release the chemical messenger dopamine may lead to the motor deficits associated with the syndrome.

Researchers have created the first mouse model of Timothy syndrome, a rare genetic disorder that causes heart defects and autism. The findings appeared 30 August in the Proceedings of the National Academy of Sciences.

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.