Spectrum: Autism Research News

Contrary to conventional wisdom, most people with fragile X syndrome express the FMR1 gene — albeit improperly.

The framework, inspired by the polygenic risk score, considers the cumulative effect of neuronal connections.

The drugs may reopen a critical window during development in which the brain can more easily adjust its connections.

The largest analysis of human samples to date, plus work in mice and zebrafish, detail the gene KMT5B’s role in brain development.

Mice and zebrafish missing the GIGYF1 gene show social traits reminiscent of autism, though the molecular underpinnings are unclear.

Connections between 13 autism-linked proteins and their binding partners in excitatory neurons implicate a new molecular pathway.

Inactivating TAOK1 prompts tentacle-like protrusions to form all over a neuron’s surface, revealing the gene’s role in molding the membrane.

The technique could be used to identify and control cells involved in autism.

Compared with their unaffected siblings and unrelated controls, children with autism harbor more copy number variants in genes that govern the circadian cycle or are associated with insomnia.

Restoring the gene, TAOK2, in mice missing an autism-linked region of chromosome 16 normalizes neuronal movement during development.