Date Thesis Awarded

4-2014

Document Type

Honors Thesis

Degree Name

Bachelors of Science (BS)

Department

Neuroscience

Advisor

Randolph Coleman

Committee Member

Joshua Burk

Committee Member

Christopher Abelt

Abstract

The purpose of this research is to further characterize the apoptotic pathways involved in a neuron affected by familial ALS. ALS is an aggressive disease that affects many people presently. However, research on neurodegeneration as it specifically pertains to ALS is limited because research on more common neurodegenerative diseases takes priority. The main objective of this research is to create a greater understanding of some of the major defining features of ALS - including mutated SOD1 gene, excitotoxicity, and organelle dysfunction. The hope is that this will help current research on the disease develop more effective treatments and, eventually, possibly even a cure.

Copper-Zinc Superoxide Dismutase (SOD1) codes for an enzyme critical for breakdown of metabolic waste – specifically reactive oxygen species such as hydrogen peroxide. Mutated forms of SOD1 lead to accumulated waste in the cells. This contributes to the development of other apoptotic factors – including apoptosome formation – within the cell. With this project, the combined effects of this waste accumulation and other outcomes of mutated SOD1 will be investigated. The ultimate goal is to identify how those effects lead to increased risk for ALS onset.

The current clinical literature on ALS has been researched in order to identify and explore a number of mutations at the SOD1 gene that are linked to the disease. The relevant literature is used to create a biochemical model of SOD1 processes and all of the involved chemical species using a freeware program, Cell Designer. The data will be quantitatively analyzed by creating a mathematical model of the biochemical model. With this mathematical model, it will be easier to identify which ones play important roles in ALS onset and progression.

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