Discovering potential combinational treatments of Amyotrophic Lateral Sclerosis (ALS) using a computational model of G93A mouse.
Lee, Albert Jong
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Instabilities in the regulatory mechanisms utilized by the superoxide dismutase 1 glycine 93 to alanine (SOD1 G93A) transgenic mouse to compensate for changes to the system have been postulated to play a considerable role in Amyotrophic Lateral Sclerosis (ALS) disease progression. However, there is currently no concrete evidence of such regulatory dysfunctions in the SOD1 G93A mouse. In order to study the complexity of ALS, a computational model of wild type (WT) mouse physiological regulation was developed using a combination of dynamic meta-analysis (DMA) and global optimization. Such model was shown to be able to predict the time dynamics of WT physiological functions. The method presented in this study will be used to construct a G93A model and can be further applied to other multifunctional diseases.