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Weaker Brain 'Sync' May Be Early Sign of Autism

June 22, 2011 — In a novel imaging study of sleeping toddlers, scientists at the University of California, San Diego Autism Center of Excellence report that a diminished ability of a young brain's hemispheres to "sync" with one another could be a powerful, new biological marker of autism, one that might enable an autism diagnosis at a very young age.


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Writing in the June 23 issue of the journal Neuron, Eric Courchesne, PhD, professor of neurosciences at the UC San Diego School of Medicine, and colleagues in Israel and Pittsburgh report that language areas located in the right and left sides of the brain are less synchronized in toddlers with autism than in toddlers displaying either language delay problems or typical development. The strength of synchronization was associated with individual language and communication abilities: the weaker the synchronization, the more severe the communication difficulties exhibited by the autistic child.

"Neural synchronization refers to the coordinated timing of neural activity across distinct brain areas," said Ilan Dinstein, PhD, a neurobiologist at the Weizmann Institute of Science in Rehovot, Israel, a member of the UCSD Autism Center of Excellence, and first author of the study.

"In a normal brain, neurons in separate areas belonging to a system with a particular function, such as vision or language, always stay in sync, even during sleep. Our study shows that in most brains of toddlers with autism this 'sync' is significantly weaker in brain areas that are responsible for language and communication abilities. Many things need to be set up right during brain development to enable normal sync between different brain areas. The wiring between the brain areas needs to be right and the neurons within each brain area need to send and receive their messages properly."

The findings, if corroborated by further research, could have significant impact, Dinstein said.

"It would be a biological rather than a behavioral measure that could be used to diagnose autism at a very young age -- around one year. The functional magnetic resonance image (fMRI) scan would not identify all of the individuals with autism, but it would be helpful in revealing the majority of individuals. The results also tell us that significant differences in the biology of language areas are apparent during very early stages of autism development. It will help focus further research into the brain differences that underlie autism."

Though the exact cause of autism remains unknown, it is hypothesized that the neurological disorder -- which is marked by impaired social and communications skills, usually manifesting itself in the first few years of life -- arises from the development of abnormal neural networks with irregular connectivity and synchronization.

Autism is a developmental disorder that progresses with time. It is currently impossible to identify autism at birth and diagnoses, which are entirely based upon observed behavioral symptoms, are typically performed only after the age of 3. These facts help make the study of how autism develops particularly challenging. Affected toddlers are prone to incessant movement and random, uncontrolled behaviors, both of which can disrupt efforts to measure brain function and structure using different imaging techniques.

To sidestep these difficulties, the UCSD scientists studied toddlers' brains at night while they were sleeping. This novel approach meant toddlers with severe autism, who are often left out of studies due to their challenging behaviors, could be included, thus permitting scientists to successfully test the strength of brain synchronization in children with different levels of development and identify the brain areas that exhibited weak synchronization in those with autism.

"We hope that this work will be one of several enlightening steps leading to a fuller understanding of the underlying biology of autism during early development," said Dinstein. "Such an understanding is critical for developing the necessary diagnostic and therapeutical tools that are so needed for successful early intervention."

Co-authors of the paper include Karen Pierce and Eric Courchesne, Autism Center of Excellence and the Department of Neurosciences, both at UCSD; Lisa Eyler, Autism Center of Excellence and Department of Psychiatry, UCSD; Stephanie Solso, Autism Center of Excellence, UCSD; Rafael Malach, Department of Neurobiology, Weizmann Institute of Science; Marlene Behrmann, Department of Psychology, Carnegie Mellon University, Pittsburgh.

Funding for this study came, in part, from grants from the National Institute of Mental Health, the National Institutes of Health, the Israel Science Foundation and the Pennsylvania Department of Health.

About autism

Autism is a neurological disorder typically appearing in the first few years of life. It affects the brain's normal development of social and communication skills. Symptoms include impaired or lost language and social skills, heightened physical sensitivities and compulsive or repetitive behaviors.

The condition is linked to abnormal biology and chemistry in the brain, but the exact causes for these abnormalities is not known, though it is likely a combination of genetic and environmental factors. The term autism broadly covers a range of complex neurodevelopment disorders known as autism spectrum disorder or ASD. The total number of children with ASD is not known, but experts estimate three to six children in every 1,000 have an ASD condition. Boys are four times more likely to have ASD than girls.

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The above story is reprinted from materials provided by University of California - San Diego, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Ilan Dinstein, Karen Pierce, Lisa Eyler, Stephanie Solso, Rafael Malach, Marlene Behrmann, Eric Courchesne. Disrupted Neural Synchronization in Toddlers with Autism. Neuron, Volume 70, Issue 6, 1218-1225, 23 June 2011 DOI: 10.1016/j.neuron.2011.04.018
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