Exploring the formation of Alzheimer's disease senile plaques in silico.
An experimental simulation environment suitable for exploring the neuroinflammatory hypothesis of Alzheimer's disease (AD) has been developed. Using scientific literature, we have calculated parameters and rates and constructed an interactive model system. The simulation can be manipulated to explore competing hypotheses about AD pathology, i.e. can be used as an experimental "in silico" system. In this paper, we outline the assumptions and aspects of the model, and illustrate qualitative and quantitative findings. The interactions of amyloid beta deposits, glial cell dynamics, inflammation and secreted cytokines, and the stress, recovery, and death of neuronal tissue are investigated. The model leads to qualitative insights about relative roles of the cells and chemicals in the disease pathology.
Edelstein-keshet
Leah
L
Department of Mathematics, University of British Columbia, Vancouver, BC, Canada,V6 T 1Z2. keshet@math.ubc.ca
Spiros
Athan
A
D000544:Alzheimer Disease / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D001921:Brain / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D003198:Computer Simulation; D016207:Cytokines / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D009457:Neuroglia / Q000473:pathology; D009474:Neurons / Q000473:pathology
D016229:Amyloid beta-Peptides; D016207:Cytokines