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Defects in crucial brain protein implicated in memory loss

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DURHAM, N.C. -- The ability to recognize familiar objects and companions is lost when levels of a protein crucial for recycling a chemical messenger in the brain are reduced, mimicking some of the symptoms of Alzheimer's disease, an international team led by Duke University Medical Center scientists has discovered.

Mice genetically engineered to have modest defects in this recycling protein display symptoms that resemble those in Alzheimer's, such as the inability to remember familiar faces, according to the researchers. The crucial protein recycles a chemical called acetylcholine that carries messages between nerves cells, the scientists said.

"By using these genetically engineered mice as models of Alzheimer's, we can learn more about the neuronal circuitry of the brain, and perhaps even discover new ways to alleviate the symptoms of this devastating disease," said senior study investigator Marc G. Caron, Ph.D., James B. Duke professor of cell biology.

The team reports its findings in the Sept. 7, 2006, issue of the journal Neuron. The research was supported by the National Institutes of Health and American Health Assistance Foundation.

Acetylcholine is a neurotransmitter that carries a number of vital signals from one nerve cell, or neuron, to another. Normally, when a signal needs to travel through the brain, neurons release acetylcholine to transport the signal across the gap, or synapse, between neurons. Acetylcholine is stored in tiny hollow spheres, called vesicles, that bud off of the end of the neurons. A kind of protein pump, called a transporter, located in each neuron controls the storage and release of acetylcholine from these vesicles, recycling the neurotransmitter back to the nerve cell vesicles in preparation for the next burst of signal.

It is this acetylcholine transporter protein that the researchers targeted by disrupting the gene that
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Contact: Marla Vacek Broadfoot
marla.broadfoot@duke.edu
919-660-1306
Duke University Medical Center
6-Sep-2006


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