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2009 Grants - Reijmers
Imaging of Memory Circuits in the Presence of Soluble Amyloid-beta
Leon Reijmers, Ph.D.
2009 New Investigator Research Grant
Beta-amyloid (or amyloid-beta) is a protein fragment at the focus of research into the causes of Alzheimer's disease. In addition to being toxic to nerve cells, beta-amyloid has been shown to cause memory impairment in mice. This effect is likely to be related to the effects of beta-amyloid on synapses, the specialized regions of nerve cells that communicate signals through the nervous system. Scientists have found that beta-amyloid impairs synaptic plasticity, a crucial mechanism by which the strength of synaptic signals changes. Synaptic plasticity is widely accepted as a mechanism of learning and memory.
Leon Reijmers, Ph.D. and colleagues have developed a unique model system that allows them to use imaging methods to visualize events occurring in nerve cells during synaptic plasticity. They have used this model system in mice to determine which nerve cells store memories for a learned task. Dr. Reijmers and colleagues now plan to use this model system to study how beta-amyloid affects the ability of nerve cells to store memories. They plan to examine which parts of the brain are most sensitive to the effects of beta-amyloid, and whether the affected nerve cells can recover after beta-amyloid is removed. Finally, the researchers plan to examine whether newly acquired memories and older memories are affected differently by the presence of beta-amyloid in the brain. These studies will advance our understanding of how beta-amyloid mediates damage in the brain, and they may suggest strategies for minimizing that damage.