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2007 Grant - Querfurth
Intraneuronal Beta-Amyloid and Synaptic Plasticity in the Prefrontal Cortex
Henry W. Querfurth, M.D., Ph.D.
Caritas St. Elizabeth's Medical Center
2007 Investigator-Initiated Research Grant
Beta-amyloid is a protein fragment that is a key component of Alzheimer pathology. Although beta-amyloid is usually thought to exert its effects from outside of cells (extracellular), it is known to first accumulate inside of the cells (intracellular).
In some parts of the brain, beta-amyloid has been shown to reduce synaptic transmission, the process by which cells send rapid signals to other nerve cells. In addition, beta-amyloid interferes with some forms of synaptic plasticity, possibly explaining some of the effects of beta-amyloid on memory.
Henry Querfurth, M.D., Ph.D., and colleagues have proposed to perform detailed studies of the effects of beta-amyloid on synaptic transmission in a region of the brain known as the prefrontal cortex. This region has received less attention than other brain regions, but it is susceptible to damage in Alzheimer's disease. Furthermore, the prefrontal cortex is thought to support a form of memory known as "working memory."
The researchers will use techniques that will enable them to record the activity of pairs of brain cells that communicate by synaptic transmission. For these studies, they will use brain tissue from mice that have been genetically modified to express features of Alzheimer's disease. These methods will enable the researchers to study how intracellular and extracellular beta-amyloid affects synaptic transmission and synaptic plasticity. The results will improve our understanding of how Alzheimer's disease affects the prefrontal cortex and working memory.