In mice and organoids lacking a neuronal protein, microglia prune synapses to excess.

New quality benchmarks for basic research involving stem cells promise to improve rigor and reproducibility, says Mosher, who helped develop the standards.

The approach, which combines CRISPR with single-cell analyses of organoids, suggests that intermediate progenitor cells are especially vulnerable to mutations associated with autism.

Experiments offer clues to why certain mutations are associated with autism in some people and not others.

The chimeric mouse model could provide a more realistic way to study microglia’s roles in brain conditions such as autism.

The changes may help explain the link between maternal infection and autism, though more research is needed.

The approach improves the function of SYNGAP1-deficient neurons in vitro, but whether it will work in people remains unclear.

A new gene therapy approach for epilepsy tamps down neural activity on demand.

The in-depth approach shows mutations in the autism-linked gene disrupt neuronal growth and communication, as well as mitochondrial gene expression.

The method yields complex organoids that more closely mimic embryonic brain development than do those cultured in other ways.