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.

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.

FMR1 loss impairs sodium channels, hindering mouse neurons from generating the electrical signals needed to transmit information.

Cells from people with fragile X syndrome overproduce — but don’t accumulate — proteins. New work suggests that excessive protein breakdown may account for this discrepancy, and explain some of the syndrome’s traits.

After a brain transplant of reprogrammed human cells, the animals can for the first time recapitulate some neuronal changes seen in people with fragile X syndrome.

People with the autism-linked syndrome lack a protein implicated in several cancers, but it’s unclear whether — or how — they are protected from malignancies.

A 341-repeat mutation from a person with fragile X does not lead to the syndrome’s traits or function the same way in mice, highlighting a need for different animal models.

An overabundance of ribosomes drives an imbalance of proteins produced from long and short genetic transcripts in a mouse model of fragile X syndrome.

Long cast in supporting roles in the brain, astrocytes are now emerging as primary players in certain characteristics of autism and related conditions.