Alzheimer's disease: analysis of a mathematical model incorporating the role of prions
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Nonlinear ordinary differential operators (34L30) Stability in context of PDEs (35B35) Initial-boundary value problems for systems of nonlinear first-order PDEs (35F61) PDEs in connection with biology, chemistry and other natural sciences (35Q92) General biology and biomathematics (92B05) Medical applications (general) (92C50)
Abstract: We introduce a mathematical model of the in vivo progression of Alzheimer's disease with focus on the role of prions in memory impairment. Our model consists of differential equations that describe the dynamic formation of {�eta}-amyloid plaques based on the concentrations of A{�eta} oligomers, PrPC proteins, and the A{�eta}-x-PrPC complex, which are hypothesized to be responsible for synaptic toxicity. We prove the well-posedness of the model and provided stability results for its unique equilibrium, when the polymerization rate of {�eta}-amyloid is constant and also when it is described by a power law.
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Cited in
(27)- A physical model for dementia
- Stability analysis of a steady state of a model describing Alzheimer's disease and interactions with prion proteins
- The interplay of biochemical and biomechanical degeneration in Alzheimer's disease
- Mathematical model of Alzheimer's disease with prion proteins interactions and treatment
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