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.

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

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.

Fragile X syndrome is a rare and devastating condition, and a risk factor for autism. New research suggesting the condition is reversible in mice has some wondering whether treatments for the syndrome ― and for some forms of autism ― could be on the horizon.