Alzheimer's disease (AD) is a progressive neurodegenerative disorder that primarily affects the elderly population over 65 years of age. In view of the United States' ageing population, it is important to understand the mechanism behind this disease to find suitable disease modifying treatments for AD.The first symptoms of AD are loss of learning and memory, not cell death, and hence we investigate these phenomena first. We observe beta-amyloid (A�) peptide's effect on kinase phosphorylation and cell viability. We find that beta-amyloid peptide induces both Tyr kinase and Src kinase phosphorylation in a time and concentration dependent manner. We also observed evidence of multiple mechanisms of Ab induced signaling activity and toxicity,and the figure depicts potential integration of signal transduction. The role of receptor versus non-receptor mediated signaling in these pathways by Ab is also investigated.Further, we propose multiple rate law models to describe A�'s interaction with cells, and fit our experimental data to these in order to find the mechanism that best describes our experimental data. We propose a plausible mechanism of Ab induced signal integration linked to neurotoxicity and long term potentiation. These results should contribute to the development of new disease modifying treatments for AD.

Pathways of A� mediated neurodegenerative pathways in cells: A model

247th National Meeting (2014)

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