Two new strains of mice carrying different mutations in the SHANK2 gene show similar autism-like behaviors but opposing effects on brain signaling, according to two independent studies published 14 June in Nature.
Seaside Therapeutics, a small biotech, and Swiss pharmaceutical giant Roche have announced a partnership to develop drugs for fragile X syndrome and autism.
A pilot project highlights how adult stem cells could be used to test and select personalized therapies.
Dysregulation of the intracellular signaling pathway RAS, a risk factor for idiopathic autism, may provide a unifying theory of the disorder. Although this is not an altogether new hypothesis, several new findings have strengthened the evidence for it considerably.
A drug that blocks a type of receptor at the junctions between neurons reverses repetitive behaviors in a mouse model of autism, according to a new study.
Altered function of a brain receptor may help explain the why infection during pregnancy raises the risk for schizophrenia in the offspring, according to an unpublished rat study presented at the 2011 Society for Neuroscience annual meeting in Washington, D.C.
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show marked improvements in brain signaling after being treated with insulin-like growth factor 1, according to unpublished findings presented Saturday at the International Congress of Human Genetics in Montreal, Canada.
Two new genetic mouse models that debuted this week show that having too many or too few copies of certain genetic regions leads to an array of symptoms reminiscent of autism.
A compound that shows promise as a treatment for fragile X syndrome alleviates repetitive behaviors in mice, but unexpectedly makes them less social.
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.