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.
The study offers a possible explanation as to why the communication centre of the brain, called the corpus callosum, is often abnormally small in people with ASD. Although most research has focused on neurons, this study also implicates oligodendrocytes.
Oligodendrocytes coat the signalling arms of a neuron with an insulating substance called myelin, which enables electrical signals to move quickly from one neuron to another. ‘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, PhD, professor and chair of genetics.
‘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 signalling through poor cellular differentiation and myelination.’