Computational model examines the pathways of Alzheimer's that strikes at...(hase kinase (GSK-3) (a protein) and amyl...)

Date:4/17/2009

hase 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.

Conclusion

Glaw's model can be used for additional pathway analysis. She views modeling as a useful way for better understanding this complex, multi-layered disease.

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Contact: Donna Krupa dkrupa@the-aps.org 703-967-2751 American Physiological Society Source:Eurekalert

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