Proteins that function at the synapse, the junction between neurons, have been strongly linked to autism. At the Society for Neuroscience annual meeting in San Diego, Mriganka Sur, professor of neuroscience at the Massachusetts institute of technology, explained how studying synapses is revolutionizing our understanding of autism.
Children with autism have an imbalance of excitation and inhibition in the brain, according to the first study to measure synchrony between brain networks using magnetoencephalography (MEG). The findings were presented Wednesday at the Society for Neuroscience annual meeting in San Diego.
In a study published last week, Huda Zoghbi’s team showed that neurons that produce a neurotransmitter called gamma-aminobutyric acid, or GABA, play a crucial role in the development of Rett syndrome. Zoghbi caught up with SFARI at the Society for Neuroscience annual meeting in San Diego to discuss the study’s implications for understanding autism.
People with autism have structural differences in the temporal cortex — a brain region involved in sound and language processing — compared with controls, according to a postmortem study presented Monday at the Society for Neuroscience annual meeting in San Diego.
Researchers have developed the first stem cell system that makes it possible to study the early development of neurons from people with Rett syndrome, a rare disorder on the autism spectrum.
Blocking the expression of the MeCP2 gene decreases the number of synapses, the junctions between neurons. It also prevents synapses from scaling up their activity to make up for the loss, according to unpublished data shown yesterday at the Society for Neuroscience annual meeting in San Diego.
A new mouse model for Rett syndrome shows that disrupting a single brain messenger can produce nearly all of the characteristic features of the syndrome, researchers report today in Nature.
Most inhibitory neurons respond in the same way to a range of visual stimulation, but a subset of them may be tuned in to specific signals, suggest two reports published in September in Neuron.
A new mouse model of Angelman syndrome that knocks out a large stretch of a key chromosome is clarifying some of the molecular mechanisms underlying the more severe forms of the disorder.
The amygdala, a brain region that regulates fear and anxiety, shows abnormal neuronal signaling in a mouse model of fragile X syndrome, according to two studies published this summer. These are the first to explore cellular defects in the region in fragile X.