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Imaging IDs Brain Neurons With Preference for Real Words

Finding could boost understanding of what causes reading disabilities


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WEDNESDAY, April 29 (HealthDay News) -- Neurons with a preference for complete, real words are located in the brain's visual word form area, U.S. researchers report.

This finding, published in the April 30 issue of Neuron, offers new insight into reading-associated brain mechanisms and may help improve understanding of reading disabilities.

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"Although some theories of reading, as well as some neuropsychological and experimental data, have argued for the existence of a neural representation for whole real words, experimental evidence for such a representation has been elusive," study senior author Dr. Maximilian Riesenhuber, of the department of neuroscience at Georgetown University Medical Center, said in a journal news release.

Previous studies had identified the visual word form area (VWFA) as being important for reading words, but researchers hadn't clearly demonstrated this brain region had a preference for real words. That was confirmed in this latest research. It included volunteers who underwent brain scans while they did tasks using written real words and nonsense words.

The brain scan results showed that neurons in the VWFA are highly selective for complete, real words. The left VWFA was the only brain area that consistently displayed this selectivity.

"These results are not just relevant for theories of reading and reading acquisitions, but also for our understanding of the mechanisms underlying experience-driven cortical plasticity in general," Riesenhuber said.

"It will be interesting in future studies to investigate how the specificity of the representation in the VWFA changes during development, and how it might differ in individuals with reading disorders," he added.

More information

Learn more about developmental reading disorders at the U.S. National Library of Medicine.



-- Robert Preidt

Copyright © 2009 ScoutNews, LLC. All rights reserved.
Last updated 4/29/2009

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SOURCE: Cell Press, news release, April 29, 2009


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