Sergiu Pasca was among the first to model autism with neurons from affected individuals, a feat that could reveal the biochemical roots of some forms of autism.

Fetal mice that have too many neurons grow to show social deficits and repetitive behaviors. The finding, reported 11 December in Cell Reports, debuts a mouse model of autism that’s based on a biological abnormality seen in some people with the disorder.

A customized microscope with moveable arms lets researchers simultaneously watch neurons fire in two areas of a mouse brain.
 

A setup that mimics early behavioral intervention reverses social and cognitive deficits seen in a mouse model of fragile X syndrome.

Mice missing the FMR1 gene only in star-shaped brain cells called astrocytes recapitulate key features of fragile X syndrome. Researchers presented the unpublished results today at the 2014 Society for Neuroscience annual meeting in Washington, D.C.

The brains of children with autism do not prune unneeded connections between neurons as they age, leaving them with too many of these neuronal links, according to a study published 21 August in Neuron.

The protein missing in fragile X syndrome is necessary for mice to respond to the stimulant cocaine, according to a study published 7 May in Neuron.

A new method for turning brains transparent and scanning them will make it easier to map neuronal circuits, according to a paper published 24 April in Cell.

Proteins that help guide neurons to their correct destination in the brain may be involved in autism, says Christopher Cowan.

Long pieces of RNA that do not code for protein have diverse and important roles in the cell and may contribute to autism risk, say Nikolaos Mellios and Mriganka Sur.