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neuronal characteristics that are strikingly similar to those of mice that completely lack the protein, according to unpublished research described Sunday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.
Deleting the Rett syndrome gene in a subset of neurons, instead of throughout the body, dramatically lowers the number of genes that are dysregulated in those neurons, according to results presented in a poster session Saturday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.
Mice missing the Rett syndrome gene MeCP2 show a gradual decline in vision, and too much inhibitory signaling in the visual cortex, according to unpublished research presented Thursday in Washington, D.C.
The Rett syndrome gene MeCP2 may subtly regulate the expression of genes across the genome by altering DNA structure.
Mice lacking a copy of SHANK3, a gene associated with autism and intellectual disability, show marked improvements in brain signaling after being treated with insulin-like growth factor 1, according to unpublished findings presented Saturday at the International Congress of Human Genetics in Montreal, Canada.
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.
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.