Among people who carry the fragile X premutation, about 14 percent of boys and 5 percent of girls meet the criteria for autism, but the ‘broad autism phenotype’ may be far more common.

A basic scientist at heart, Hollis Cline has spent decades pushing the boundaries of what researchers can see in the brain. Her persistence has led to a deeper understanding of how some autism-linked genes influence brain development.

The protein, FMRP, shapes cell signaling near synapses but switches to regulate genes in the cell body, according to new research.

Clues that problems with mitochondria contribute to autism have been accumulating for decades. In the past five years, a mutant mouse and a flurry of findings have energized the field.

Two new methods make it possible to delete long sections of the genome, expanding the reach of CRISPR gene editing.

Activating certain receptors in the amygdala — a treatment that runs counter to a leading theory of what causes the condition — can reverse some traits in rats.

Autism involves mutations in noncoding portions of the genome in at least 3 percent of people with the condition. The mutations occur in regions that help regulate known autism-linked genes.

The stubborn lack of treatments for fragile X syndrome — a leading cause of inherited intellectual disability and autism — is spurring researchers to revise clinical trial techniques and revisit old drug candidates.

Over the past century, scientists have used a variety of animal models to advance their understanding of the developing brain and autism.

In the past two decades, some autism researchers have turned to simple animals, such as roundworms, fruit flies and zebrafish, for their investigations. Others have sought answers from experiments with frogs, birds and even octopuses.