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

Scientists’ desire for evidence-based medical inquiry runs headlong into an apparently immovable obstacle: the U.S. Drug Enforcement Agency.

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.