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

The mutations disrupt protein translation as well as the cell’s skeleton, according to a new study.

Knocking down the gene that codes for the proteins normalizes the vocalizations.

Many genes related to the condition play a role in the internal scaffolding of cells, and cytoskeletal disruptions can affect neurodevelopment and behavior.

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.

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

Faulty mTOR signaling, implicated in syndromic forms of autism, also hinders cells grown from people with idiopathic autism or autism-linked deletions on chromosome 16.

Therapies that target the circuit could boost social activity, new findings suggest.

ADNP and SHANK3 proteins may bind together and alter a neuron’s internal scaffold, hinting at a mechanism that, when disrupted, may underlie several forms of autism.

Pups born to mothers that experience low oxygen during sleep have overactive mTOR signaling, which has been linked to some forms of autism.