Inherited genetic factors for autism influence brain development, new studies of autistic children and their younger siblings reveal.

The cells’ altered proliferation rates hint at ways to diagnose and potentially treat autism earlier.

By as early as age 2, autistic children appear to have a smaller salience network and a larger default mode network, among other differences, than children without the condition.

Neurons with a faulty copy of SETD1A, a gene tied to autism and schizophrenia, show structural abnormalities and altered connectivity patterns.

Strategies to replace or compensate for mutated copies of the TCF4 gene could lead to treatments for this profound form of autism, a new study suggests.

Drugs such as LSD act primarily on the serotonin system, which is implicated in autism — and some autistic people who experiment with psychoactive compounds report enhanced social connections, among other benefits. But researchers have more questions than answers.

Increased white-matter maturation tracks with stronger language abilities later in childhood, but the relationship with cortical thickness is less clear.

The size of the cerebral cortex seems to depend on when neural progenitor cells multiply or differentiate into glial cells and neurons.

The new resource is the first to chart human brain development from before birth to 100 years of age.

Animals with different autism-linked mutations share disruptions to the mTOR signaling pathway, pointing to a potential molecular mechanism for the atypical cerebellar development seen in some autistic people.