The anxiety and trouble with social skills seen in people with autism may originate outside of the brain, in neurons that govern touch.

An early-stage treatment for eye cancer reverses memory problems in a mouse model of fragile X syndrome.

Boosting levels of the fragile X protein FMRP in astrocytes reverses features of fragile X syndrome in mice.

The same autism-linked mutation can lead to dramatically different behaviors in rats and mice.

Glowing particles called ‘Sticky-flares’ can light up RNAs, the molecular blueprints for protein production, in living cells. Using these flares, researchers can plot the paths of specific RNAs through a cell.

Researchers have discovered an enzyme that lowers brain levels of FMRP, the protein missing in people with fragile X syndrome. Blocking the enzyme may ease fragile X symptoms in people with the disorder who have low levels of FMRP and mild symptoms.

Blocking an enzyme involved in learning and memory corrects brain abnormalities and improves memory in fly and mouse models of fragile X syndrome.

A human gene gives mice bigger brains, and people with autism weigh in on that white or blue dress.

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

The memory and sleep troubles that accompany fragile X syndrome originate in a glitch in insulin signaling, suggests an unpublished study of fruit flies presented today at the 2014 Society for Neuroscience annual meeting in Washington, D.C. The study points to a widely available diabetes treatment for the syndrome.