A treatment that targets the genetic defect in tuberous sclerosis prevents autism-like symptoms in mice at 6 weeks of age — the mouse equivalent of adolescence. Researchers presented the unpublished results yesterday at the 2014 Society for Neuroscience annual meeting in Washington, D.C.
Mice modeling autism have trouble integrating different kinds of sensory information such as sight, sound and touch. A study published 31 July in Neuron reports that an imbalance between signals that calm neurons and those that excite them leads to these sensory problems.
Mutations in a gene linked to intellectual disability and sometimes autism may lead to a permanent boost in brain activity, according to a study published 18 June in Neuron.
A long-awaited report, published today in Nature, confirms that with access to tens of thousands of genomes, researchers can identify common genetic risk factors for a complex neuropsychiatric disorder.
A “beautiful” new study traces a complex repetitive behavior in a mouse model of autism to a subset of neurons in one brain region.
There are no available medications for treating autism’s core symptoms, but there are several candidates in clinical trials. Jeremy Veenstra-VanderWeele describes the factors researchers must take into account when developing drugs for the disorder.
Proteins that help guide neurons to their correct destination in the brain may be involved in autism, says Christopher Cowan.
FMRP, the protein absent or mutated in fragile X syndrome, aids in strategic elimination of neuronal connections during brain development in mice, according to a study published 26 February in The Journal of Neuroscience.
Following disappointing results from two clinical trials, the Swiss pharmaceutical company Novartis announced on 24 April that it will stop development of a drug candidate for fragile X syndrome.
Deleting MeCP2 from a subset of neurons that mediate inhibitory signals recapitulates many of the symptoms of Rett syndrome in mice. Conversely, expressing the gene only in that subset, but not in the rest of the brain, protects the mice from some of those same symptoms. The results were published last week in Nature Neuroscience.