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Brain Adapts to Age-Related Eye Disease

Neurons seek input from undamaged areas to compensate, study finds


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TUESDAY, March 3 (HealthDay News) -- When macular degeneration causes one to start losing his or her sight, the affected neurons simply start seeking visual input from other, non-affected parts of the eye, Massachusetts Institute of Technology researchers report.

"This study shows us one way that the brain changes when its inputs change. Neurons seem to want to receive input: When their usual input disappears, they start responding to the next best thing," senior author Nancy Kanwisher, of MIT's McGovern Institute for Brain Research, said in an university news release.

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The researchers found when the cells in the fovea, the part of the retina responsible for the central field of vision, were damaged by macular degeneration (MD) -- the neuron attached to them begin responding to stimuli in an undamaged section -- a type of internal reorganization of the eye's visual map as opposed to the cortex's work being shifting to other neurons.

"Our study shows that the changes we see in neural response in people with MD are probably driven by the lack of input to a population of neurons, not by a change in visual information-processing strategy," Kanwisher said.

The findings are published in the March 4 issue of the Journal of Neuroscience.

Macular degeneration, the most common form of adult blindness, affects almost 2 million people in the United States. Patients often compensate for lack of central vision by rolling their eyes upward so they can utilize the preferred retinal locus (PRL), an undamaged area under and adjacent to the affected part of the retina.

"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex," Kanwisher said.

More information

The U.S. National Eye Institute has more about macular degeneration.



-- Kevin McKeever

Copyright © 2009 ScoutNews, LLC. All rights reserved.
Last updated 3/3/2009

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SOURCE: Massachusetts Institute of Technology, news release, March 3, 2009


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