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

The animals recall fear more readily if a set of inhibitory neurons in the hippocampus is switched on.

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

Deleting a copy of the gene TBX1 depletes the fatty myelin insulation that surrounds neurons and reduces cognitive speed in mice.

A potential new gene therapy delivered via a single injection mimics ratios of proteins normally found in cells.

Activating certain receptors in the amygdala — a treatment that runs counter to a leading theory of what causes the condition — can reverse some traits in rats.

Social memory, which may be altered in autism, depends on serotonin-sensitive neurons that send signals from the medial septum to the hippocampus.

Jolting a bundle of nerve fibers deep in the brain restores learning and memory in mice with mutations of the autism-linked gene CDKL5.

Misaligned gene expression maps suggest that some autism-linked genes play distinct roles in mouse and human brains.

Mice missing a copy of the autism-linked gene NRXN1 appear to perceive some time intervals as shorter than control mice do, according to a new study.