FMRP, the protein missing in fragile X syndrome, is needed for the birth of new neurons, for regulating the translation of RNA into protein, and for maintaining the structural integrity of spiny neuronal projections, according to several new studies.

Variations in two genes needed to form connections between brain cells may be associated with autism spectrum disorder, according to a study published 25 March in Molecular Autism. Some variants in the genes seem to increase susceptibility to autism, whereas others protect children from developing the disorder.

Among animal models of autism, the mouse reigns supreme. But could much simpler species — flies, bees, worms, fish — also teach us about the disorder?

Researchers are tinkering with mouse models to investigate the function of a protein that helps wire neurons together and that has repeatedly been linked to autism. Three such reports of the protein, neuroligin-1, have appeared this year.

Two independent teams have discovered key molecular steps in the way a single gene disrupts the connections between neurons in individuals with Angelman syndrome. Because the gene, UBE3A, has also been linked to autism, the findings could help scientists understand and treat a range of neurodevelopmental disorders.

Several studies in the past year in people, mice and honeybees have tied autism to a protein that helps neurons communicate. Problems with the protein, neurexin 1, are associated with a wide range of autistic behaviors, such as impaired social interactions, anxiety and problems with learning and memory.

To examine protein interactions inside brain cells, scientists typically zero in on one gene at a time. A new method described in today’s Nature simultaneously measures expression of the whole genome.

The human brain holds a mind-boggling 100 billion neurons. Mapping their connections is the lofty goal of the Human Connectome Project, a $30 million scheme sponsored by the National Institutes of Health.

Young mouse models of fragile X syndrome show a significant lag in the development of synapses, the connections between neurons, according to a study published in Neuron. The findings suggest that a similar mistiming may be responsible for the sensory problems — such as hypersensitivity to touch and sound — sometimes seen in people with fragile X syndrome.

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.