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.

Scientists have discovered that neurexins — proteins linked to autism — bind to a wide variety of molecules at the junction between neurons. In this complicated system, the breakdown of any one of the parts could lead to improper cell signaling, ultimately giving rise to disease.

Children with fragile X syndrome show abnormal growth in several brain structures during the first few years of life, according to the first study to track how the disease unfolds in the brain during early development.

There are several short periods during development in which our brains are ‘plastic’ — meaning that neuronal connections appear and disappear depending on how much they are used. Researchers may have found a way to reopen those learning windows.

Researchers have found a higher density of several types of interneurons — nerve cells that connect sensory and motor neurons in the brain— in postmortem brain tissue from individuals with autism, compared with healthy controls. The findings appear in the February issue of Acta Neurologica Scandinavica.

Scientists have for the first time found direct evidence that defects in the GABA receptor sometimes give rise to autism, according to research published 24 November in Molecular Psychiatry.

Autism may be the result of faulty wiring that occurs during early brain development, according to two independent studies that looked at the origins of circuit disruption.

A pathway involved in language development is increasingly proving to be important in autism, suggest a series of new studies on cellular and behavioral aspects of the disorder.

Selectively disrupting an autism-related gene in cultured human neurons causes a dramatic imbalance of excitation and inhibition in cell signaling, according to unpublished results presented today at the Society for Neuroscience meeting in Chicago.