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2006 Grant - Magrane
Synaptic Damage from Intraneuronal Abeta Accumulation
Jordi Magrane, Ph.D.
Weill Medical College of Cornell University
New York, New York
2006 New Investigator Research Grant
One of the earliest pathological features of Alzheimer's disease is the loss of synapses, specialized structures that facilitate communication between neurons in the brain. Why these synapses degenerate is unclear, but many scientists believe that beta-amyloid, the small protein fragment that has become synonymous with the disease, may be responsible.
One theory suggests that a build up of beta-amyloid inside neurons eventually leads to the collapse of synapses. Confirming that theory requires a much better understanding of how beta-amyloid behaves inside neurons, but that has proven to be a difficult task. One of the main problems with studying neurons is having them make proteins to order.
Jordi Magrane, Ph.D., has developed a system whereby specific proteins are rapidly and efficiently produced inside neurons. The key is to infect cultured neurons with viruses that carry the genetic code for the protein of interest. Magrane and colleagues have used this system to produce beta-amyloid inside cultured neurons and, in so doing, have linked the small protein fragment to increased cellular stress and decreased survival. She now plans to use this same system to examine if and how beta-amyloid may affect the function or maintenance of synapses. This work may lead to new insights into the potential toxic properties of beta-amyloid.