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.

Among people who carry the fragile X premutation, about 14 percent of boys and 5 percent of girls meet the criteria for autism, but the ‘broad autism phenotype’ may be far more common.

The protein, FMRP, shapes cell signaling near synapses but switches to regulate genes in the cell body, according to new research.

The stubborn lack of treatments for fragile X syndrome — a leading cause of inherited intellectual disability and autism — is spurring researchers to revise clinical trial techniques and revisit old drug candidates.

Steve Warren co-discovered the genetic mechanism that underpins fragile X syndrome and was a generous, inspiring mentor to many.

Brain cells from the cerebellums of mice that model tuberous sclerosis show dampened levels of proteins controlled by FMRP, the protein missing in fragile X syndrome.

Elizabeth Berry-Kravis has spent decades uncovering molecular clues to fragile X syndrome and crafting trials of treatments. Her efforts are paying off.

Cara Westmark has spent the past year building the case that a drug designed for fragile X syndrome might help coronavirus patients, too.

The Spectrum team highlights five topics that distinguished autism research in 2020: diversity in data, gene therapies, subtyping, social circuitry and the ‘autism gene’ debate.