MeCP2, the gene associated with Rett syndrome, has widely variable effects on mouse brains depending on the mutation it carries, according to unpublished results presented Tuesday at the 2013 Society for Neuroscience annual meeting in San Diego.

Rett syndrome affects many cellular pathways, but correcting just one of these with drugs approved for other purposes may be enough to alleviate symptoms of the disorder. This was the message from two presentations Tuesday at the 2013 Society for Neuroscience annual meeting in San Diego.

Bone marrow transplants, which have been shown to arrest symptoms of Rett syndrome in young mice, have little effect on older mice, according to preliminary results presented Monday at the 2013 Society for Neuroscience annual meeting in San Diego. The findings suggest that this approach may not be a viable treatment for those who already have symptoms of the disorder.

Insulin-like growth factor 2, a hormone involved in fetal growth, reverses abnormal social behaviors, repetitive behaviors and memory impairments in BTBR mice, a popular model of autism. The unpublished results were presented Monday at the 2013 Society for Neuroscience annual meeting in San Diego.

Rat models of autism have a weak and sluggish brain response to speech sounds, but behavioral training can improve their performance. The unpublished results, presented Sunday at the 2013 Society for Neuroscience annual meeting in San Diego, suggest that a similar approach may benefit people with the disorder.

Watch the complete replay of Beth Stevens discussing the link between immune cells in the brain, neuronal junctions and autism. Submit follow-up questions.

Mutations in a gene that plays a role in producing cholesterol in the body increase the risk for autism, suggesting therapies for some people with the disorder, according to research presented in a poster Tuesday at the Autism Consortium’s 2013 Research Symposium.

SHANK3, one of the strongest candidate genes for autism, has the potential to be a molecular entry point into understanding the synaptic, developmental and circuit origins of the disorder.
 

Mutations in the autism-linked protein NHE6 may block the development of neuronal junctions by interfering with a growth factor called BDNF, according to a study published 2 October in Neuron.

A virus that ferries healthy copies of the Rett syndrome gene across the blood-brain barrier can reverse symptoms in female mice that model the disorder, according to a report published 21 August in the Journal of Neuroscience. The approach is the closest yet to simulating a workable treatment for the autism-related disorder.