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Holding a mirror to brain changes in autism

Date:
March 2, 2012
Source:
Elsevier
Summary:
Impaired social function is a cardinal symptom of autism spectrum disorders (ASDs). One of the brain circuits that enable us to relate to other people is the “mirror neuron” system. This brain circuit is activated when we watch other people, and allows our brains to represent the actions of others, influencing our ability to learn new tasks and to understand the intentions and experiences of other people. This mirror neuron system is impaired in individuals with ASD and better understanding the neurobiology of this system could help in the development of new treatments.

Impaired social function is a cardinal symptom of autism spectrum disorders (ASDs). One of the brain circuits that enable us to relate to other people is the "mirror neuron" system. This brain circuit is activated when we watch other people, and allows our brains to represent the actions of others, influencing our ability to learn new tasks and to understand the intentions and experiences of other people.

This mirror neuron system is impaired in individuals with ASD and better understanding the neurobiology of this system could help in the development of new treatments.

In their new study, Dr. Peter Enticott at Monash University and his colleagues used transcranial magnetic stimulation to stimulate the brains of individuals with ASD and healthy individuals while they observed different hand gestures. This allowed the researchers to measure the activity of each individual's mirror neuron system with millisecond precision in response to each observed action.

They found that the individuals with ASD showed a blunted brain response to stimulation of the motor cortex when viewing a transitive hand gesture. In other words, the mirror neuron system in the ASD individuals became less activated when watching the gestures, compared to the healthy group. In addition, among people with ASD, less mirror neuron activity was associated with greater social impairments. This finding adds to the evidence that deficits in mirror neuron system functioning contribute to the social deficits in ASD.

This finding also directly links a specific type of brain dysfunction in people with autism spectrum disorder to a specific symptom. This is important because "we do not have a substantial understanding of the brain basis of autism spectrum disorder, or a validated biomedical treatment for the disorder," said Dr. Enticott. "If we can develop a substantial understanding of the biology of specific symptoms, this will allow us to develop treatments targeted specifically to the symptoms."

"This study is an example of the effort to break down the component problems associated with autism spectrum disorder and to map these problems on to particular brain circuits," commented Dr. John Krystal, editor of Biological Psychiatry.

Enticott added, "We are currently investigating whether non-invasive brain stimulation can be used to improve mirror neuron activity in autism spectrum disorder, which would have substantial potential therapeutic implications."


Story Source:

The above story is based on materials provided by Elsevier. Note: Materials may be edited for content and length.


Journal Reference:

  1. Peter G. Enticott, Hayley A. Kennedy, Nicole J. Rinehart, Bruce J. Tonge, John L. Bradshaw, John R. Taffe, Zafiris J. Daskalakis, Paul B. Fitzgerald. Mirror Neuron Activity Associated with Social Impairments but not Age in Autism Spectrum Disorder. Biological Psychiatry, 2012; 71 (5): 427 DOI: 10.1016/j.biopsych.2011.09.001

Cite This Page:

Elsevier. "Holding a mirror to brain changes in autism." ScienceDaily. ScienceDaily, 2 March 2012. <www.sciencedaily.com/releases/2012/03/120302132317.htm>.
Elsevier. (2012, March 2). Holding a mirror to brain changes in autism. ScienceDaily. Retrieved July 28, 2014 from www.sciencedaily.com/releases/2012/03/120302132317.htm
Elsevier. "Holding a mirror to brain changes in autism." ScienceDaily. www.sciencedaily.com/releases/2012/03/120302132317.htm (accessed July 28, 2014).

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