Autism is not just a brain disorder

Autism is not just a brain disorder

Autism is not just a brain disorder

Autism is not just a brain disorder, according to new research from the journal Cell.

Autism spectrum disorder (ASD) is a range of complex neurodevelopment disorders. This disorder is characterized by social impairments, trouble with communication, and restricted, repetitive stereotyped patterns of behavior. According to the National Institutes of Health, experts estimate that 1 out of 88 children will have autism spectrum disorder.

ASD is generally thought to be caused by a deficiency in brain development. However, the new study shows that some aspects of the disorder including anxiety, social abnormalities, and how touch is perceived are linked to another part of the nervous system, which is the peripheral nerves found in the limbs, digits, and the rest of the body. These nerves carry sensory information to the brain.

An underlying assumption has been that ASD is solely a disease of the brain, but we’ve found that may not always be the case,” says senior author David Ginty, a Professor of Neurobiology at Harvard Medical School and a Howard Hughes Medical Institute Investigator. “Advances in mouse genetics have made it possible for us to study genes linked to ASD by altering them only in certain types of nerve cells and studying the effects.”

The study abstract summarized the following study details:

Patients with autism spectrum disorders (ASDs) commonly experience aberrant tactile sensitivity, yet the neural alterations underlying somatosensory dysfunction and the extent to which tactile deficits contribute to ASD characteristics are unknown. We report that mice harboring mutations in Mecp2, Gabrb3, Shank3, and Fmr1 genes associated with ASDs in humans exhibit altered tactile discrimination and hypersensitivity to gentle touch. Deletion of Mecp2 or Gabrb3 in peripheral somatosensory neurons causes mechanosensory dysfunction through loss of GABAA receptor-mediated presynaptic inhibition of inputs to the CNS. Remarkably, tactile defects resulting from Mecp2 or Gabrb3 deletion in somatosensory neurons during development, but not in adulthood, cause social interaction deficits and anxiety-like behavior. Restoring Mecp2 expression exclusively in the somatosensory neurons of Mecp2-null mice rescues tactile sensitivity, anxiety-like behavior, and social interaction deficits, but not lethality, memory, or motor deficits. Thus, mechanosensory processing defects contribute to anxiety-like behavior and social interaction deficits in ASD mouse models.

The study showing that autism is not just a brain disorder was published in the journal Cell.

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1. “Autism Fact Sheet.” National Institute of Neurological Disorders and Stroke (NINDS). National Institutes of Health, n.d. Web. 13 Jun. 2016.
2. “Mouse Study Suggests Autism Is Not Just a Disease of the Brain.” EurekAlert! Cell Press, n.d. Web. 13 June 2016.
3. “Peripheral Mechanosensory Neuron Dysfunction Underlies Tactile and Behavioral Deficits in Mouse Models of ASDs.” Cell. Cell, n.d. Web. 13 June 2016.

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