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Alzheimer’s disease (AD) is a neurodegenerative disease. It is a growing concern, demanding the attention of families, scientists, and pharmaceutical companies due to its devastating impacts on patients. The disease is believed to be triggered by pathogenic amyloid beta protein (Aβ) formations in the brain. In order to understand the protein production and the plaque formation in the AD brain, we specifically focused on the ‘Amyloid Cascade Hypothesis,’ which explains the biological pathways and the players in the disease. Focusing on the macro-side, we modelled the progression of AD from neurodevelopment (healthy brain) to neurodegeneration (the disease state) by using the agent based computer simulation program called COBWEB. Our model begins with healthy, developing neurons thriving in the hippocampus and cerebrospinal fluid (CSF) working efficiently. The brain ages throughout the adulthood phase. The onset of the disease and its progression is modelled with plaque formation, a decline in neuron counts, and an inefficient cleaning mechanism close to the end of the experiment. We conclude that our model fulfills its purpose: to provide a visual contrast between health and disease through the slow progression of AD in real time, increasing one’s understanding of this illness. Its accuracy is attributed to Aβ plaque formation, neuronal death, and CSF deterioration. Future projects include testing, designing, and refining new treatments using this model, diminishing the barrier to entry for new ideas, and providing a new tool for teaching AD. La maladie d’Alzheimer (MA) est une maladie neurodegenerative. Elle est un souci croissant, exigeant l’attention des familles, des scientifiques et des societes pharmaceutiques en raison de ses effets devastateurs sur les patients. Nous pensons que la maladie est provoquee par la formation pathogenique de la proteine beta amyloide (As) dans le cerveau. Afin de comprendre la production de la proteine et la formation de plaques dans le cerveau d’un patient atteint de MA, nous avons mis l’accent specifiquement sur l’hypothese de la cascade amyloide, ce qui explique les voies biologiques et les acteurs impliques dans la maladie. En nous concentrant sur la macroscopie, nous avons modelise la progression de la MA du debut du neurodeveloppement (le cerveau en bonne sante) a la neurodegenerescence (l’etat de la maladie) en utilisant le programme de simulation numerique base sur un agent appele COBWEB. Notre modele commence avec des neurones qui se developpent normalement, grandissant dans l’hippocampe et le liquide cephalo-rachidien (LCR) et travaillant efficacement. Le cerveau vieillit tout au long de la phase adulte. L’apparition de la maladie et de sa progression est modelisee avec la formation des plaques, une diminution du nombre neurones, et un mecanisme de nettoyage inefficace pres de la fin. Nous concluons que notre modele repond a son but de fournir un contraste visuel entre la sante et la maladie a travers la lente progression de la MA en temps reel, ce qui augmente notre comprehension de la MA. Sa precision est attribuee a la formation de plaques As, la mort neuronale et la deterioration du LCR. Les projets futurs incluent des tests, la conception et le raffinage de nouveaux traitements en utilisant ce modele, ce qui diminue la barriere a l’entree pour de nouvelles idees, et de fournir un nouvel outil pour enseigner la MA.

Modelling neurodevelopment, neurodegeneration, and amyloid beta aggregation in the context of Alzheimer's using COBWEB