Researchers Identify Protein Module Involved in Autism

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Researchers Identify Protein Module Involved in Autism
Researchers Identify Protein Module Involved in Autism

A multidisciplinary team of researchers have identified a molecular network made up of many of the genes that have been shown to contribute to autism spectrum disorders.

The network helps identify shared molecular pathways and protein interactions across the wide swath of gene mutations that are associated with autism. The goal is to identify novel candidate genes of the disease that could benefit future studies and eventually, targeted therapies.

Michael Snyder, PhD, professor at the Stanford Center for Genomics and Personalized Medicine, and colleagues used the BioGrid database of protein and genetic interactions to generate the interactome and identify a module comprised of 119 proteins that are enriched for known autism genes. The researchers performed genome sequencing on 25 patients and exome sequencing on 500 patients, and confirmed the module's involvement in autism. The gene expressions in the module were examined with the Allen Human Brain Atlas.

The researchers noted the importance of the corpus callosum and oligodendroctye cells as contributors to autism spectrum disorders.

"Much of today's research on autism is focused on the study of neurons and now our study has also revealed that oligodendrocytes are also implicated in this disease," said Jingjing Li, postdoctoral fellow at the Stanford Center for Genomics and Personalized Medicine. "In the future, we need to study how the interplay between different types of brain cells or different regions of the brain contribute to this disease."

The researchers hypothesize that disruptions in parts of the corpus callosum interfere with circuitry that connects the two hemispheres of the brain, giving rise to different phenotypes of autism. 

Reference

  1. Li J et al. Mol Syst Biol. 2014; doi:10.15252/msb.20145487.
  2. EurekAlert press release. Available here: http://www.eurekalert.org/pub_releases/2014-12/e-mni122514.php 
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