title: A mathematical model of insulin resistance in Parkinson's disease.
abstract: This paper introduces a mathematical model representing the biochemical interactions between insulin signaling and Parkinson's disease. The model can be used to examine the changes that occur over the course of the disease as well as identify which processes would be the most effective targets for treatment. The model is mathematized using biochemical systems theory (BST). It incorporates a treatment strategy that includes several experimental drugs along with current treatments. In the past, BST models of neurodegeneration have used power law analysis and simulation (PLAS) to model the system. This paper recommends the use of MATLAB instead. MATLAB allows for more flexibility in both the model itself and in data analysis. Previous BST analyses of neurodegeneration began treatment at disease onset. As shown in this model, the outcomes of delayed, realistic treatment and full treatment at disease onset are significantly different. The delayed treatment strategy is an important development in BST modeling of neurodegeneration. It emphasizes the importance of early diagnosis, and allows for a more accurate representation of disease and treatment interactions.
authors.affiliation: Department of Chemistry, Integrated Science Center, 540 Landrum Drive, The College of William and Mary, Williamsburg, VA 23187, USA. Electronic address: embraatz@email.wm.edu.
authors.forename: Elise M
authors.initials: EM
authors.lastname: Braatz
authors.affiliation: Department of Chemistry, Integrated Science Center, 540 Landrum Drive, The College of William and Mary, Williamsburg, VA 23187, USA. Electronic address: racole@wm.edu.
authors.forename: Randolph A
authors.initials: RA
authors.lastname: Coleman
mesh_terms: D003198:Computer Simulation; D004298:Dopamine / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000378:metabolism / Q000473:pathology; D007333:Insulin Resistance; D016631:Lewy Bodies / Q000378:metabolism / Q000473:pathology; D008954:Models, Biological; D018384:Oxidative Stress; D010300:Parkinson Disease / Q000150:complications* / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D010766:Phosphorylation; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism; D016875:tau Proteins / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D016875:tau Proteins; D048051:p38 Mitogen-Activated Protein Kinases; D004298:Dopamine
keywords: Computational biology; Delayed treatment; Insulin resistance; Neurodegenerative disease; Parkinson’s disease; Type-II diabetes mellitus