Autism May Result From Communication Defect Between Brain Halves

the Psychiatry Advisor take:

Stanford University School of Medicine researchers say that some cases of autism may be the result of poor communication between the two halves of the brain.

Michael Snyder, PhD, chair of genetics at the school, and colleagues analyzed the human interactome — a large network of interacting proteins — as well as sequencing genomes and examining gene expression in people with autism.

The corpus callosum, the brain’s communication center, is frequently abnormally small in those with autism, the researchers report in the journal Molecular Systems Biology. Their work also indicates that oligodendrocytes, which coat signaling arms of neurons with myelin to allow electrical signals to move more quickly between neurons, also play a role in autism.

“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,” Snyder said in a statement. “Until now, we've suspected that autism could be the result of defects in the neurons themselves. Now it appears that the oligodendrocytes can contribute to the problem by inhibiting neuronal signaling through poor cellular differentiation and myelination."

The researchers also discovered a group of 119 proteins involved in nerve cell communication in patients with autism. That module has genes involved in the development and functioning of oligodendrocytes.