A new tool could help decipher the brain circuits underlying aversion to social touch, which is common in people with autism.

Synaptic changes in the brain region could drive a core trait of fragile X syndrome, a new mouse study suggests.

A protective pathway that pauses protein synthesis is muted in a mouse model of fragile X syndrome, according to a new study.

Brain scans of hundreds of infants suggest that up to 80 percent of those with autism have unusual amounts of cerebrospinal fluid. Researchers are studying how this might contribute to the condition.

This month’s issue of the Null and Noteworthy newsletter breaks down some negative results involving prenatal exposures, an experimental treatment for Angelman syndrome, and the role that age at autism diagnosis plays in subsequent outcomes, and more.

Contrary to conventional wisdom, most people with fragile X syndrome express the FMR1 gene — albeit improperly.

The approach prompts cultured cells to correct the genetic mutation in fragile X syndrome using their own DNA repair system, but it still needs to be tested further.

Many genes related to the condition play a role in the internal scaffolding of cells, and cytoskeletal disruptions can affect neurodevelopment and behavior.

A shift in astrocyte secretions may explain the atypical firing patterns of neurons derived from people with fragile X syndrome.

Autistic children taking the drug showed improvements in some behaviors but not in their social skills.