Alterations in inhibitory circuits and difficulties in social recognition characterize mice missing one copy of DYRK1A, a gene linked to autism.

Increasing or reducing the levels of the UBE3A gene, which is associated with autism and autism-related syndromes, results in altered patterns of synaptic pruning — a process that snips away brain cell connections.

When combined with tissue-inflation methods, the microscope can image axons without the need for tissue slicing, the researchers say.

Many genes related to the condition play a role in the internal scaffolding of cells, and cytoskeletal disruptions can affect neurodevelopment and behavior.

The paper marks the second retraction for one of the co-authors.

The map diagrams more than half a million neuronal connections in the first complete connectome of Drosophila and holds clues about which brain architectures best support learning.

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.

Many autism-linked genes are somehow tied to cilia, the tiny hair-like sensors that stud a cell’s surface. But the question remains whether, and how, cilia differences contribute to the condition.

The in-depth approach shows mutations in the autism-linked gene disrupt neuronal growth and communication, as well as mitochondrial gene expression.

The growth differences vary between autistic boys and girls and are most apparent among children with prominent social difficulties.