Genes

Mice with autism- or schizophrenia-linked mutations only in the anterodorsal thalamus have problems with long-term and working memory.

Mounting evidence suggests that autism often involves upsets in homeostatic plasticity, a set of processes neurons use to stabilize their activity. These disruptions result from a range of autism-linked mutations and may help to explain the condition’s famed heterogeneity.

Brain cells from the cerebellums of mice that model tuberous sclerosis show dampened levels of proteins controlled by FMRP, the protein missing in fragile X syndrome.

The same genetic factors may underlie both autism and autistic people’s tendency to have sleep problems, such as insomnia.

The finding that MDMA and an experimental serotonin agonist increase sociability across six different model mice suggests that disparate autism-linked mutations converge on the same underlying pathways.

Deleterious mutations in an autism-associated gene can make neurons hyperexcitable, raising the risk of epileptic seizures.

Spontaneous mutations in parts of the genome that regulate gene EBF3 appear to contribute to autism risk.