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.
A defect in communication between the two halves of the brain may be responsible for some cases of autism, according to a study by researchers at the Stanford University School of Medicine.
They came to their conclusions by analyzing what’s called the human interactome — a vast network of interacting proteins — and by sequencing genomes and analyzing gene expression patterns in individuals with autism.
The study offers a possible explanation as to why the communication center of the brain, called the corpus callosum, is often abnormally small in people with the condition. Although most research has focused on neurons, this study also implicates the oligodendrocytes in the disorder. Oligodendrocytes coat the signaling arms of a neuron with an insulating substance called myelin, which enables electrical signals to move quickly from one neuron to another.