Date of Award

7-6-2022

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

School of Biological Sciences

First Advisor

Alysia Vrailas-Mortimer

Abstract

Oxidative stress and mitochondrial dysfunction have been linked to multiple age-related diseases including common neurodegenerative diseases Alzheimer's disease (AD) and Parkinson’s disease (PD). A gene found to regulated oxidative stress and aging is a stress response gene p38 MAPK (p38K). Oxidative stress arises when the over production of reactive oxygen species (ROS) from within the cell or from environmental stimuli outweighs its clearance by antioxidants. This cascade leads to DNA damage, mitochondrial damage, and cell death. Mitochondrial dysfunction and oxidative stress are markers for biological aging. As we age mitochondrial DNA becomes more sensitive to damages and mutations. When the mitochondria become damaged there is a network of genes involved in its degradation. These proteins include PINK1, a protein kinase that is processed inside of the mitochondria, and parkin, an E3-ubiquitin ligase that will poly-ubiquitinate the mitochondria for degradation. In addition, these genes are found to be linked to the onset of Parkinson’s Disease. Parkinson’s Disease is a mostly sporadic disease with environmental influencing disease onset. Copper, a heavy metal used throughout our bodies, is believed to be one of these influences. Copper homeostasis is regulated in the body by my proteins, including ATP7. This work explores the relationship between copper homeostasis, Parkinson’s disease, and oxidative stress in the context of aging.

Comments

Imported from Burkhart_ilstu_0092N_12223.pdf

DOI

https://doi.org/10.30707/ETD2022.20221020070310603289.999997

Page Count

51

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Available for download on Saturday, October 05, 2024

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