A mouse model of Rett syndrome that mimics a mutation seen in people shows many features of the disorder, such as hand clasping, according to a study published 27 November in Nature Neuroscience.

HMGN1, a protein that regulates gene expression, leads to social deficits and hyperactivity when expressed at elevated levels in mice, according to a study published 9 December in the Journal of Biological Chemistry. This effect may result from HMGN1 dampening MeCP2 expression, the study suggests.

In China, some parents of children with developmental disorders seek help — sometimes hundreds of miles from home — but have trouble getting it because of poor healthcare infrastructure, high costs, long lines and doctors’ lack of awareness.

Researchers have derived neurons from stem cells to investigate mutations that lead to Rett and fragile X syndromes.

The etiology of autism may be best understood as an impairment of neuronal circuits, specifically interneurons that dampen signals in the brain, says neuroscientist Gordon Fishell.  

The brains of mice that model Rett syndrome are smaller than normal overall and have differences in specific regions similar to those seen in people with the disorder, according to unpublished research presented Wednesday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.

Researchers have charted the expression of tiny pieces of RNA in postmortem brain tissue from people with autism, according to unpublished research presented Tuesday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.

A large scientific research company debuted seven new rat models of autism Tuesday evening in Washington, D.C. Two of the models, one lacking FMR1 and the other lacking NLGN3, show some unexpected new characteristics.

Mice with a mutation in the Rett syndrome gene are more social than controls, according to a study published 11 September in Behavioral Genetics. The results, based on detailed observation of social behavior, support previous studies showing that Rett syndrome mouse models do not have severe social deficits.

Mice that have an excess of the Rett syndrome protein MeCP2 have biochemical and neuronal characteristics that are strikingly similar to those of mice that completely lack the protein, according to unpublished research described Sunday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.