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

In this edition of Null and Noteworthy, scientists find little to be excited about in research on biomarkers for neurodevelopmental conditions.

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.

Chung, a clinical and molecular geneticist, plans to continue serving as principal investigator of two large research projects involving cohorts of people with autism and related neurodevelopmental conditions.

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.

This week’s newsletter considers tweets about the assumptions baked into brain-imaging studies; the reach of brain waves; and a diet-based intervention for a rare autism-linked condition.

The dual diagnosis frequently co-occurs with anxiety, depression and developmental and language delays.

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.

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.