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.

Mouse models of fragile X syndrome show defects in two kinds of potassium channels — ubiquitous pores that control the flow of electrical current across neurons — in a brain area that processes sound, according to two papers published this summer.

You’ll never hear Jacqueline Crawley talk about an ‘autistic mouse’. In fact, in her keynote address at IMFAR in May, she implored the audience to never use those two words in the same sentence.

Researchers have uncovered an important molecular piece of a learning mechanism that occurs at the junction between neurons. The findings, which may help understand how the brain is disrupted in disorders such as autism, appear in the 24 June issue of Neuron.

Scientists have for the first time captured a dynamic picture of brain defects in young mouse models of fragile X syndrome. The findings appeared in June in the Journal of Neuroscience.

Families affected by fragile X syndrome can let out a modest cheer this week: the largest-ever randomized trial of a drug to treat the syndrome has just cleared its second phase.

The biology of obsessive-compulsive disorder becomes even more baffling with the release of two new mouse models, each implicating a different type of brain cell.

A study of a rare form of epilepsy found in Amish groups adds heft to the idea that mTOR — a much-studied hub in a massive network of brain cell proteins — is an important biochemical player in autism.

Mice engineered to carry a well-known risk factor for schizophrenia show disruptions in the connections between two brain regions that coordinate memory and learning. And these disruptions directly cause problems with working memory — the ability to actively hold information and to recall that information to make a decision, according to a study published in Nature.

A new model that compares how the same genes behave in different organisms could help researchers identify previously unknown candidates for diseases such as autism. The model, published in the Proceedings of the National Academy of Sciences, takes advantage of the genetic overlap between humans and simpler organisms to discover genes associated with complex diseases.