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.

The treatment eases the animals’ sleep troubles, suggesting it has clinically meaningful effects beyond what was thought to be a critical window in early life.

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.

The gene, linked to a little-known condition called Weiss-Kruszka syndrome, prevents embryonic stem cells from deviating from their neuronal destiny.

Cells from people with fragile X syndrome overproduce — but don’t accumulate — proteins. New work suggests that excessive protein breakdown may account for this discrepancy, and explain some of the syndrome’s traits.

Inactivating TAOK1 prompts tentacle-like protrusions to form all over a neuron’s surface, revealing the gene’s role in molding the membrane.