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

UBE3A, a key gene associated with both autism-linked conditions, can explain most — but not all — of the syndromes’ atypical neuronal properties.

The map diagrams more than half a million neuronal connections in the first complete connectome of Drosophila and holds clues about which brain architectures best support learning.

Exposing neurons to valproic acid, a well-known environmental risk factor for autism, disrupts their ability to generate different proteins from the same gene.

Altered expression of TSC2 and the mTOR pathway reshape the formation of certain synapses between inhibitory and excitatory neurons in mice.

Cells from people with fragile X syndrome overproduce — but don’t accumulate — proteins. New work suggests that excessive protein breakdown may account for this discrepancy, and explain some of the syndrome’s traits.

Memories from Diering’s life trace the rising star’s scientific path from raising lizards as a child and later exploring home brewing to heading a lab that investigates memory, sleep disturbances and early development in animals with autism-linked mutations.

Many autism-linked genes are somehow tied to cilia, the tiny hair-like sensors that stud a cell’s surface. But the question remains whether, and how, cilia differences contribute to the condition.

Rumbaugh, who studies how the autism-linked gene SYNGAP1 shapes brain development, describes how he has embraced coastal living and which aspects of his career he wouldn’t do over.

A new method that merges tissue expansion, light-sheet microscopy and automated image segmentation can reconstruct neural circuits in about a week.