Soluble proteins band together into temporary complexes to travel to the tips of neurons, according to a study published 12 May in Neuron. The study provides the first evidence-based model for slow, directed neuronal transport, answering a long-standing question in the field.

Spontaneous and inherited mutations in SHANK3 both inhibit the protein’s role at synapses, the junctions between neurons, according to a study published 24 May in Molecular Psychiatry.

Several targeted trials on drugs that treat fragile X syndrome are under way. But accurate endpoints to measure the drugs’ effectiveness are crucial, argues developmental and behavioral pediatrician Randi Hagerman.

Researchers have identified hundreds of previously unknown connections between proteins involved in autism spectrum disorders, according to a report published last week in Science Translational Medicine.

Three new studies analyzing genetic data from families in which just one child has autism have found the strongest evidence yet that rare new mutations contribute to the disorder.

Deletions on a segment of chromosome 11 are associated with autism, attention problems and obesity, according to a study published in the June issue of the American Journal of Medical Genetics Part A.

Mice with a mutation in SHANK3, a leading autism candidate gene, show moderate social defects, including less-than-normal interest in other mice. The findings, published 27 May in Cell, suggest that mutations in different sites on the gene can lead to different behaviors. This paper was retracted on 17 January 2013. Associate director of research Alan Packer discusses the implications of the retraction here.

A new study provides the first functional link between the schizophrenia risk gene DISC1 and two candidate genes for autism. DISC1 significantly alters expression of NRXN1 and NRXN2 at key phases of development, according to a brief report in the June issue of Molecular Psychiatry.

Two networks of genes are abnormally expressed in the brains of people with autism, according to a study published today in Nature.

MeCP2, the protein that’s missing or mutated in Rett syndrome, is crucial for remodeling neural circuits in response to vision, according to a study published in April in Neuron.