Charting the structure and function of the brain’s many circuits may unravel autism’s mysteries.
By zapping mouse brains with blue and yellow light beams, scientists have manipulated the animals’ social behaviors and bolstered a popular theory of what causes autism.
The first study to sequence more than 100 genes on the X chromosome in people with autism or schizophrenia has turned up some promising leads.
A study using action potentials, the electrical impulses that trigger signaling, shows that neurons lacking MeCP2, the Rett syndrome protein, have stronger neuronal signals compared with controls, according to a study published in the July Journal of Neurophysiology.
Infants with fragile X syndrome spend more time looking at a toy before switching their attention elsewhere than do healthy controls, according to a study published 1 July in the Journal of Autism and Developmental Disorders.
A variant of neurexin 1, a gene linked to both autism and schizophrenia, is associated with less brain matter than normal in healthy individuals, according to a study published 8 June in PLoS ONE.
The protein missing in people with fragile X syndrome regulates the activity of more than 800 other proteins, including some key players in autism, according to a study published 22 July in Cell. Many of these autism-associated proteins cluster on either side of the synapse, the junction between neurons.
An elegant microscopy technique reveals that neurons can regulate how quickly they recycle chemical messengers, according to a study published in July in Nature Neuroscience. This process is believed to be the limiting step in the speed of signaling across neuronal junctions.
Small fragments of RNA, called microRNAs, can fine-tune the levels of proteins at the junctions between neurons in response to cell signals, according to a study published 10 June in Molecular Cell.
Broken rules are even more distressing to people with autism than being excluded, according to a new study.
