Mice that model Angelman syndrome or have a duplication of the 15q11-13 chromosomal region have aberrant brain levels of the chemical messenger serotonin, according to a study published 16 August in PLoS One.

Researchers are beginning to tease apart how dosage of genes within the 15q11-13 chromosomal region contributes to autism symptoms.

Concerned by researchers’ lack of access to a valuable mouse model of autism, a nonprofit advocacy group is dedicating a chunk of its limited resources to the creation of a freely available version.

Delicate dosage issues are just one complication of developing gene therapy for neurodevelopmental disorders.

Mice lacking a functional copy of UBE3A, the gene missing or mutated in people with the rare developmental disorder Angelman syndrome, show less inhibitory activity than controls do, according to research published 7 June in Neuron.

Researchers typically use only one ‘cohort,’ a group of about three dozen mice, for a given set of experiments. When others repeat the experiments with a different set of animals, sometimes the results hold up, and sometimes they don’t.

Two studies report abnormalities in the system that mediates the body’s response to stress in two mouse models of autism-related diseases: Angelman syndrome and Rett syndrome. The results were published in the April issue of Human Molecular Genetics.

Despite funders’ requirements to share mouse models after publication, many researchers hoard the animals for the good of their labs — and that could have an adverse effect on the field as a whole.

A cancer drug shows promise as a treatment for Angelman syndrome, according to a study published today in Nature.

Researchers have identified 12 duplications or deletions of DNA regions that are transmitted along with autism in families with a history of the disorder. The results were published 7 October in PLoS One.