New findings from researchers at the Stanford University School of Medicine and Lucile Packard Children's Hospital, and colleagues, shed light on the neural basis of memory defects in Down syndrome and suggest a new strategy for treating the defects with medication. The study, which was conducted in mice, is the first to show that boosting norepinephrine signaling in the brains of mice, which have been genetically engineered to mimic Down syndrome, improves their cognition. Norepinephrine is a neurotransmitter that nerve cells use to communicate. The scientists said that their findings raise the possibility that restoring norepinephrine-mediated neurotransmission could reverse cognitive dysfunction in Down syndrome. "If you intervene early enough, you will be able to help kids with Down syndrome to collect and modulate information," said Dr. Ahmad Salehi, the first author of the study. "Theoretically, that could lead to an improvement in cognitive functions in these kids." The results give "a ray of hope and optimism for the Down syndrome community for the future," said Dr. Melanie Manning, director of the Center for Down Syndrome at Lucile Packard Children's Hospital. Dr. Manning was not a part of the research team. "It's very exciting," she said. "We still have a long way to go, but these are very interesting results." This report was featured as the cover story of the November 18 issue of Science Translational Medicine. [Press release] [Science Translational Medicine abstract]Login Or Register To Read Full Story