Compared with their unaffected siblings and unrelated controls, children with autism harbor more copy number variants in genes that govern the circadian cycle or are associated with insomnia.

Common variants in five regions of the genome may determine whether someone has one condition versus the other.

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

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.

The long-standing link between maternal infection during pregnancy and having a child with autism may reflect common genetic or environmental factors instead.

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.

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

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