The model enables the study of autism-linked genes at the earliest stages of neural development.

Brain cell clusters serve as drug screens and reveal connectivity differences for autism-linked conditions, two new models show.

People with dup15q syndrome and those with idiopathic autism have similar patterns of altered gene expression in early brain development and later in life.

The developmental models have advantages over natural embryos and other synthetic models, such as organoids, but present technical and ethical challenges.

The transplanted cells integrate into living animals’ neural circuitry and influence behavior.

What these genes do and how they affect autism depends on when in development they’re studied, despite what classic ‘gene ontology’ analyses say.

The method, called Orgo-Seq, reveals that a deletion of genes on chromosome 16 increases the proportion of immature neurons and neural precursors in brain organoids derived from people with the mutation.

Long cast in supporting roles in the brain, astrocytes are now emerging as primary players in certain characteristics of autism and related conditions.

A handful of scientists are committed to advancing research on the autism-related genetic conditions their own children have.

Strategies to replace or compensate for mutated copies of the TCF4 gene could lead to treatments for this profound form of autism, a new study suggests.