Faulty communication between the halves of the brain could be the cause of some cases of autism, according to a Stanford School of Medicine study that points autism research in a new direction.

“This is our first glimpse of autism’s underlying biological framework, and it implicates a cell type and region of the brain that have not been extensively studied in this disease,” said Michael Snyder, professor and chair of genetics and the senior author of the study.

Rather than directly analyzing the cells of the corpus callosum, which facilitates communication between the two hemispheres of the brain, Snyder and his fellow researchers analyzed previously published data on the human interactome, a giant network of interacting proteins. They then sequenced the genomes and exomes of autistic individuals to confirm their conclusions.

They found that problems may arise not only from defects in neurons themselves, as was previously suspected, but from mutated oligodendrocytes, which create the insulating myelin sheath that covers neurons’ arms and speeds the transmission of electrical signals.

This may explain why the corpus callosum is often unusually small in autistic individuals.

The study will not necessarily lead to immediate new therapy methods, according to Joachim Hallmayer, one of its co-authors, but it may make it easier to divide patients into smaller, more homogenous groups based on which genes are mutated.

Contact Abigail Schott-Rosenfield at aschott ‘at’ stanford.edu.