Deleting CYFIP1, a gene within a region linked to Angelman syndrome and autism, in mice leads to symptoms reminiscent of fragile X syndrome, according to a study published 10 August in PLoS One.
Amphetamines and other compounds with stimulant properties may improve social behaviors in a subset of individuals who have autism with hyperactivity, says Jill Silverman.
As the central organ regulating maternal-fetal interactions, the placenta is perfectly positioned to mediate environmental and genetic risk factors during prenatal development. It may also relay risk factors for autism to the fetus, says Paul Patterson.
Researchers have developed an index that can predict the age of developing interneurons, which inhibit signals in the brain, according to a study published 24 August in PLoS One. They then used this measurement to show that interneurons are immature in autism brains.
Mice that lack the autism-linked gene neuroligin-3 show similar deficits in neuronal connections to those seen in fragile X syndrome, an inherited form of mental retardation, according to research published 13 September in Science. Restoring the gene in adolescent mice reverses the problem, suggesting a potential pathway for treatment.
A New York Times opinion column on 25 August suggested that at least some cases of autism could be considered inflammatory disorders. But this theory is still in its infancy.
A compound called baclofen restores the balance between different types of brain signals and alleviates autism-like behaviors in mice, according to a study published 17 July in Translational Psychiatry. A similar drug called arbaclofen is in clinical trials as a treatment for autism and fragile X syndrome.
Compounds that target the receptor for the chemical messenger serotonin could help treat fragile X syndrome, according to a study published 17 July in Biological Psychiatry.
Researchers have homed in on the brain region thought to be responsible for the autism-like symptoms that can accompany Dravet syndrome, a rare epilepsy disorder, according to research published Wednesday in Nature.
Deleting the Rett syndrome gene from mature mouse brains leads to the same neurological and behavioral symptoms as deleting it during a key developmental stage, according to a study published 18 July in the Journal of Neuroscience.