such as "Introduction", "Conclusion"..etc
Alzheimer’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, 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 variables—genetic mutations in
proteins and “tau” tangles—might 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
Brain Plaque: A Major Instigator?
The proteins presenilin-1 (PS1) (a mutated gene found in familial
AD) and glycogen synthase kinase (GSK-3) (a protein) and amyloid beta
(Aβ) plaque (amino acids that are found in large quantity in AD) were
studied to quantitatively examine their roles in the development of
Alzheimer’s pathology. The elements (in the form of existing research
data) were applied to the model, which was constructed of kinetic
equations developed from literature searches, and analyzed the
interactions of the proteins and complexes under various scenarios. The
model is a first-of-its-kind approach to modeling, understanding and
predicting Alzheimer’s pathways.
Results: No Link Between A Protein and Plaques, Tangles
GSK3 had a large effect on tangle formation, but very little on the
plaques. Activating GSK3 was not found to be sufficient to cause
changes in the brain to the extent seen in Alzheimer’s patients.
However, overproduction of GSK3 as opposed to activation may be able to
cause those changes. Nor was there any link found between amyloid beta
plaque and tau tangles. The main conclusion of the model so far is that
no single change to the system can cause Alzheimer’s disease. Multiple
changes, such as a PS1 mutation combined with GSK3 over-activation can,
however. A multi-pronged approach to treating the disease may be best.
Glaw’s model can be used for additional pathway analysis. She views
modeling as a useful way for better understanding this complex,
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