In a video interview at the 2011 Society for Neuroscience annual meeting in Washington, D.C., Caroline Blanchard describes some of the unusual behaviors that suggest that the BTBR mouse is a good model for autism.
Drugs that act on the adrenaline system can alleviate autism-like symptoms in a rat model of the disorder, according to unpublished research presented Sunday in Washington, D.C.
A new tool called BrainSpan is providing researchers with exquisitely detailed windows into when genes are expressed and where they are located as the brain develops. An overview of the project was presented Sunday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.
In a video interview at the 2011 Society for Neuroscience annual meeting in Washington, D.C., Joseph Buxbaum discussed the importance of mice with mutations in SHANK3, a leading autism candidate gene.
Neurexins, autism-linked proteins that organize synapses, the junctions between neurons, function in only a subset of cells in the brain, according to data presented in a poster Monday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.
A protein involved in the cascade of interactions at the junctions between neurons points to a potential therapy for fragile X syndrome, according to unpublished data presented at the 2011 Society for Neuroscience annual meeting in Washington, D.C.
The fragile X protein FMRP helps make proteins at the synapse, the junction between neurons, even when the genetic instructions for doing so are located far away in the nucleus, says Kimberly Huber.
Connections between the amygdala — a deep nub involved in processing emotions — and other parts of the brain are more numerous in children than in adults, according to unpublished research presented at the 2011 Society for Neuroscience annual meeting in Washington, D.C.
Scientists are analyzing more than 7,000 studies of functional magnetic resonance imaging to refine the role of various regions in the brain, according to unpublished work presented Monday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.
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neuronal characteristics that are strikingly similar to those of mice that completely lack the protein, according to unpublished research described Sunday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.
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