Protein networks identified in autism-linked genetic deletion
The OTUD7A gene, which may account for some traits in people missing a segment of chromosome 15, appears to interact with several known autism-linked genes.
Charting the structure and function of the brain’s many circuits may unravel autism’s mysteries.
The OTUD7A gene, which may account for some traits in people missing a segment of chromosome 15, appears to interact with several known autism-linked genes.
Researchers know little about the ways genetic variants affect development in the infant brain. Knickmeyer, who launched the Organization for Imaging Genomics in Infancy, has spent the past five years trying to close the gap.
The finding calls into question differences between autistic and non-autistic people on a decades-old theory-of-mind test involving interacting geometric shapes.
Five autism-linked genes widely known as chromatin regulators appear to also shape the cell’s internal skeleton.
Exposing neurons to valproic acid, a well-known environmental risk factor for autism, disrupts their ability to generate different proteins from the same gene.
Connections between 13 autism-linked proteins and their binding partners in excitatory neurons implicate a new molecular pathway.
Altered expression of TSC2 and the mTOR pathway reshape the formation of certain synapses between inhibitory and excitatory neurons in mice.
A new measure shows how greatly movement influences associations between traits and brain activity, revealing abundant false positives and false negatives.
CRISPR-edited prairie voles that lack receptors for the so-called “social hormone” still bond with their mate and pups, raising questions about the molecule’s role.
Cells from people with fragile X syndrome overproduce — but don’t accumulate — proteins. New work suggests that excessive protein breakdown may account for this discrepancy, and explain some of the syndrome’s traits.