NEW ORLEANSAlzheimer's disease (AD) is a tragic disease that robs an individual of their memory and mental capacity. One in eight people over the age of 65 now suffer from the disease and one in two people over 85 are diagnosed with the disease. Contrary to popular belief, Alzheimer's does not only affect the elderly. Familial Alzheimer's disease (FAD), an offshoot of the disease, affects those as young as 30.
Alzheimer's is a complex disease, and so too are the attempts to explain it. One way to understand how the brain works to cause the disorder is by using computational modeling, (a series of equations) to characterize an individual aspect that is important to the disease. Biomedical engineers Lydia S. Glaw and Thomas C. Skalak, Ph.D., of the Department of Biomedical Engineering, University of Virginia, Charlottesville, have created a model to examine the role of certain proteins in the development of the disease. Their findings are contained in the study entitled A Computational Model of the Role of Presenilin-1 and Glycogen Synthase Kinase-3 in Familial Alzheimer's Disease. They will present their findings at the 122nd Annual Meeting of the American Physiological Society (APS; www.the-aps.org/press), which is part of the Experimental Biology 2009 scientific conference. The meeting will be held April 18-22, 2009 in New Orleans.
The researchers constructed a simple computational model to measure plaques and tangles and their influence in causing FAD. The model tested the hypothesis that certain variablesgenetic mutations in proteins and "tau" tanglesmight be predicative of the development of the disease. The main hypothesis that the model tested was the idea that GSK3 is a link between amyloid beta buildup and tau tangle development.
Brain Plaque: A Major Instigator?
The proteins presenilin-1 (PS1) (a mutated gene found in familial AD) and glycogen synt
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American Physiological Society