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

Mice missing the autism-linked SHANK2 and SHANK3 genes in their retrosplenial cortex have trouble distinguishing between novel and familiar mice.

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.

Restoring the gene, TAOK2, in mice missing an autism-linked region of chromosome 16 normalizes neuronal movement during development.

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.

The technique involves editing the cellular instructions to make MECP2 protein and partially restores its levels in the brainstem.

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.

The brains of mice carrying different mutations in the autism-linked gene TBR1 display different molecular changes yet similar structural changes, resembling those previously found in autistic people with TBR1 mutations.

Mice with a mutated copy of SHANK3 fail to establish normal sleep patterns during development.

Sleep disruption early in life has long-lasting consequences for mice missing a copy of the autism-linked gene SHANK3.