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Fragile X, Down Syndromes Linked to Faulty Brain Communication,,Stanford Researcher Finds

e said. "But these results unequivocally show that the pre-synaptic cells are the important ones in this defect."

The result paralleled the researchers' earlier finding in the brains of the mice with Down syndrome symptoms: more connections are made by fewer cells. "We believe that these reduced-complexity networks are the basis for the mental retardation that occurs with both syndromes," Madison said.

If so, the problem is rooted in early development. Synapse formation appears at first to be completely disordered, with connections between neurons making random paths like hairline cracks racing across a breaking sheet of ice. But as the person or animal begins to learn and remember, the more well-trodden paths, or cracks, connect in purposeful, yet unique ways.

"No two nerve cells will always be connected in the same way in different people," said Madison. "But populations of cells will develop similar connections as the developing brain practices using its own network. If we can compensate for the synaptic deficiency of the mutant cells, we may begin to start to think about ways to increase the mental capacity of patients with Down syndrome or Fragile X."

The study was funded by the National Institutes of Mental Health and Stanford's Down Syndrome Research Center.

Stanford University Medical Center integrates research, medical education and patient care at its three institutions -- Stanford University School of Medicine, Stanford Hospital & Clinics and Lucile Packard Children's Hospital at Stanford. For more information, please visit the Web site of the medical center's Office of Communication & Public Affairs at http://mednews.stanford.edu.

Contact

Stanford University Medical Center
Krista Conger, 650-725-5371 (Print Media)
kristac@stanford.edu
M.A. Malone, 650-723-6912 (Broadcast Media)





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