Findings on microglia and other brain cell types bolster the animal’s validity as a model system for the condition.

An analysis of 11 cortical regions shows anterior-to-posterior shifts in gene expression linked to autism.

The gene, YTHDF2, has not previously been linked to autism.

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

Collecting brain scans from thousands of people can be challenging in autism research; data-sharing and collaborative efforts can help drive results that stand up to statistical scrutiny.

Mice missing the autism-linked SHANK2 and SHANK3 genes in their retrosplenial cortex have trouble distinguishing between novel and familiar mice.

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

Common variants in five regions of the genome may determine whether someone has one condition versus the other.

Restoring the gene, TAOK2, in mice missing an autism-linked region of chromosome 16 normalizes neuronal movement during development.

After a brain transplant of reprogrammed human cells, the animals can for the first time recapitulate some neuronal changes seen in people with fragile X syndrome.