Mice missing the autism gene NLGN3 have altered social behaviors and brain responses to the hormone oxytocin, both of which improve after treatment with a drug that helps regulate protein production.

Lowering the levels of a protein called tau, best known for its involvement in Alzheimer’s disease, improves behavior in two mouse models of autism.

Neurons in mice that lack an autism gene called CNTNAP2 do not differentiate well between social and nonsocial smells — an issue that seems to stem from haphazard neuronal firing.

Loss of certain neurons on one side of the brain may explain why some autistic people are hypersensitive to touch.

Injecting cells called interneurons into the brains of a mouse model of autism restores typical social behavior. But the reason for this effect is a puzzle.

Forecasts for this year’s Nobel Prizes include several researchers whose work is relevant to autism.

An analysis of four mouse models negates certain assumptions underlying the signaling imbalance theory of autism.

A brain region that orchestrates responses to social cues and aids decision-making may be off tempo in autism.

Autism is predominantly genetic in origin, but a growing list of prenatal exposures for mother and baby may sway the odds.

Lattice-like structures that surround neurons may be overly abundant — or scarce — in brain regions of three autism mouse models.