Q&A

Autism is undoubtedly on the rise, but we may never be able to fully explain why, says Maureen Durkin.
 

An autism-linked gene controls the number of neurons in the developing brain. Freda Miller and David Kaplan say the finding points to a new role for the gene in the early embryo.

Clinicians saw autism signs in children with mutations in a cancer pathway long before sequencing studies made the connection, says Katherine Rauen.

Understanding how oxytocin works in the brain will help researchers cut through the hype surrounding the infamous ‘love hormone’ and translate it into a treatment for autism, says Larry Young.

Treatments for fragile X syndrome may be more successful if they block direct targets of the key missing protein, says Eric Klann.

Understanding why some children appear to outgrow their autism diagnosis may provide clues about the biology of the disorder but shouldn’t dictate treatment decisions, says Deborah Fein.

Drugs designed to treat fragile X syndrome have yet to show substantial benefits in people. But rather than abandon them, child neurologist Elizabeth Berry-Kravis suggests a new way to measure their effectiveness.

Existing autism therapies do little to lower the lifetime costs of having the disorder, so clinicians should consider more efficient and inexpensive alternatives, says David Mandell.

Names such as autism, schizophrenia and intellectual disability are ‘umbrella’ terms that muddy the search for the true cause of an individual’s symptoms, says Eric London. He plans to come up with an alternative diagnostic scheme for developmental disabilities over the next two years.

Finding people who have an autism-linked mutation but no apparent symptoms may be the key to identifying drug targets for the disorder, says Thomas Insel, director of the National Institute of Mental Health.