These short reports from Spectrum journalists highlight some of the autism-related findings that caught our attention at the meeting this past week.

Animal models of autism rooted in exposure to maternal antibodies hint at different mechanisms.

Dysfunctional circuits and a rogue sodium channel in the brainstem may explain the disordered breathing pattern seen in children with Pitt-Hopkins syndrome, a form of autism.

Compared with a previous mouse strain, a new model better reflects some of the difficulties that people with a rare autism-related syndrome experience, and may help identify biomarkers of the syndrome.

Social memory, which may be altered in autism, depends on serotonin-sensitive neurons that send signals from the medial septum to the hippocampus.

Even partial loss of the gene impairs the mouse brain’s ability to respond to sensory experiences, which may explain why people with SYNGAP1 mutations tend to have learning difficulties and a high pain tolerance.

The possibility of microbial treatments for autism has inspired a burst of research and nascent clinical trials, but new research suggests these efforts rest on shaky scientific ground.

A drug that helps promote gene expression reduces repetitive behaviors and improves memory and sociability in a mouse model of autism.

The first animal model of MYT1L syndrome suggests that fast-maturing neurons lead to the unusually small brains, social deficits and other traits seen in people with the condition.

Mice exposed to unusually low levels of the placental hormone allopregnanolone in the womb show atypical brain development and autism-like behaviors.