Scott describes his work on sound processing differences in the brains of zebrafish that model fragile X syndrome.

Data from two separate research teams suggest the cells are key to sensory hypersensitivity in fragile X syndrome.

One drug blocks mTOR signaling, and the other stops the blocker from acting anywhere in the body but the brain, lowering the potential for side effects.

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.

Non-neuronal brain cells called astrocytes secrete proteins that seem to hamper the growth of neurons in people with autism-related syndromes. These proteins could be new drug targets, Allen says.

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.

A researcher’s existential crisis led to a scientific breakthrough.

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.