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Many causes for learning lags in tumor disorder
Date:12/21/2012

distribute dopamine and leading to reduced attention in those mice.

The new research suggests that both sides may be right.

In the latest study, postdoctoral fellow Kelly Diggs-Andrews, PhD, found that the branches of dopamine-producing nerve cells that normally extend into the hippocampus are shorter in Nf1 mice. As a result, dopamine levels are lower in that part of the brain.

Charles F. Zorumski, MD, the Samuel B. Guze Professor and head of the Department of Psychiatry, showed that the low dopamine levels disrupts the ability of nerve cells in the hippocampus to modulate the way they communicate with each other. These communication adjustments are a primary way the brain creates memories.

Researchers then found that giving Nf1 mice L-DOPA, which increases dopamine levels, restored their nerve cell branch lengths to normal and corrected the hippocampal communication defect. L-DOPA also eliminated the memory and learning deficits in these mice.

"These results and the earlier findings suggest that there are a variety of ways that NF1 may cause cognitive dysfunction in people," Gutmann says. "Some may have problems caused only by increased RAS function, others may be having problems attributable to reduced dopamine, and a third group may be having difficulties caused by both RAS and dopamine abnormalities."

To customize patient therapy, Gutmann and his colleagues are now working to develop ways to quantify the contributions of dopamine and RAS to NF1-related learning disorders.


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Contact: Michael C. Purdy
purdym@wustl.edu
314-286-0122
Washington University School of Medicine
Source:Eurekalert

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