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M. Paul Murphy has worked as a researcher in the areas of aging and neurodegenerative disease for more than 20 years. His focus on AD began while he was a post-doctoral fellow at the Mayo Clinic in Jacksonville, FL. Since moving to the University of Kentucky in 2005, he has authored or co-authored 53 peer reviewed manuscripts, including notable recent publications in the Annals of Neurology and the American Journal of Pathology (2012).
Since his early career, Dr. Murphy has involved in developing several of the mouse models that are now well known and widely used in the AD field.
My lab is interested in how normal aging, genetics and environment conspire to cause Alzheimer’s disease (AD). The amyloid-β (Aβ) peptide, which deposits in the brain, is believed to cause AD. Our research is based around a working model where we hypothesize that, in most people, AD is caused by a loss of the normal regulation of the two enzymes involved in generating Aβ, β- and γ-secretase (top panel). These enzymes cut Aβ out of a larger membrane protein. In normal individuals, a small amount of Aβ is made as a byproduct of normal cellular metabolism. Cells secrete the peptide, and it is then degraded. In AD, a variety of things cause β- and γ-secretase to become more active. This leads to the generation of more Aβ, which overwhelms the brain’s clearance capacity. This eventually leads to disease. We use a variety of methods in cellular and molecular biology to understand why this happens, in the hope that this will one day lead to effective treatments.
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