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Mathematical Modeling for the Pathogenesis of Alzheimer’s Disease

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‘Mathematic Modeling for The Pathogenesis of Alzheimer’s Disease’
It is possible to apply mathematical models to the determination of the pathogenesis relating to Alzheimer’s Disease (AD). A large extent of this situation is made possible by the aspect of dynamic cross-talks involving multiple cell types which occur in the aging process. The application of a mathematic model is used in the definition of differential rate equations of various cross-talks. These includes neurons, microglia, amyloid-β (Aβ), and astroglia. The activation of inflammation involving microglia has demonstrated to be a key component used in progressive neurodegeneration. The role of this article is to review the mathematical modeling technique used to develop AD.Differential rate equation is used to determine the population of the cell and Aβ molecules. Experimental data are examined through the cross-talks involving microglia for purposes of appropriate refinement of the model. Through this, there is a concrete implementation of realistic parameters which are incorporated in the equation involving differential rates. The activation of microglia is part of the clinical trials which requires its inflammation towards the formation of the disease. Microglia is considered to be the component of immune macrophages inside of the brain tissue which expresses reactive oxygen species and pro-inflammatory mediators. It is at this stage where microglia stimulates the survival of neurons thus preventing the proliferation of astroglia.

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The case of increased positive and negative responses of macroglia cells leads to the process of neurodegeneration altering the functioning of AD.
It can thus be seen that a mathematic model for developing AD involves the combination of differential rate equations and the inflammation of the microglia. The involvement of differential rate equation helps in the determination of the call and Aβ molecules for the AD. The inflammation of microglia leads to the neurodegeneration which alters the functioning leading to AD.

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