A cellular pathway that helps neurons grow and move during fetal development may drive the changes in head size in some autistic people.

Mice with an autism-linked deletion in chromosome 16 show abnormalities in their blood vessels and circulation.

Clusters of brain cells — so-called ‘mini-brains’ grown in the lab — may help researchers understand how large stretches of duplicated or deleted DNA affect the brain.

The absence of several interacting genes may underlie the developmental problems seen in people missing a segment of chromosome 16.

Boosting the levels of the chemical messenger serotonin makes mice that model autism more social — and brings new hope to a shelved theory in autism.

New results implicate an enzyme called ERK in the consequences of missing a segment of chromosome 16.

A protein proves crucial to spatial memory in mice, genes in the 16p11.2 chromosomal region interact in fruit flies’ eye development, and having more autism features tracks with decreased responsiveness to direct gaze.

Mice and people missing a copy of a chromosomal region called 16p11.2 show similar patterns of weak brain connections.

Female mice may compensate for the loss of a piece of chromosome 16 better than male mice do.