FMR1 loss impairs sodium channels, hindering mouse neurons from generating the electrical signals needed to transmit information.

The approach removes methyl tags from the gene and shields it from other silencing factors without changing the gene itself, raising hopes for a new treatment.

Both human and mouse progenitor cells with the alterations struggle to become neurons and instead express genes that are typically active only in muscle or the heart.

Five autism-linked genes widely known as chromatin regulators appear to also shape the cell’s internal skeleton.

Exposing neurons to valproic acid, a well-known environmental risk factor for autism, disrupts their ability to generate different proteins from the same gene.

Connections between 13 autism-linked proteins and their binding partners in excitatory neurons implicate a new molecular pathway.

The findings put genetic background forward to help explain autism’s heterogeneity.

Elsevier’s retractions focus on peer review and conflicts of interest.

A new measure shows how greatly movement influences associations between traits and brain activity, revealing abundant false positives and false negatives.

CRISPR-edited prairie voles that lack receptors for the so-called “social hormone” still bond with their mate and pups, raising questions about the molecule’s role.