Date of Defense
12-13-2013
Date of Graduation
12-2013
Department
Biological Sciences
First Advisor
Robert Eversole
Second Advisor
Jerry Colca
Third Advisor
Charles Ide
Abstract
Neurodegeneration leads to the loss of normal anatomy and physiology of the neuronal system in a human body. The hallmark of most neurodegenerative diseases is abnormal folding and accumulation of proteins within neuronal cell bodies that is not present in healthy people. These changes in normal protein metabolism often lead to neuronal cell death and failure of the affected regions of the central nervous system. Abnormal protein accumulation may be attributed to dysfunctional mitochondria and damage by reactive oxygen species. In addition to causing altered protein accumulation, dysfunctional mitochondria and an excess of reactive oxygen species also lead to errors in glucose metabolism, which create problems in energy production and insulin signaling. The problems in these processes are targets for therapeutic techniques to find treatments for neurodegeneration and include insulin sensitizing compounds, and antioxidants. No treatments have yet been found successful to rid a person of neurodegeneration completely; however, progress has been made towards targeting the mitochondria and reactive oxygen species to halt the progress of neurodegenerative diseases in humans.
Recommended Citation
Farina, Leah, "Mitochondrial Dysfunction and Reactive Oxygen Species in Neurodegeneration" (2013). Honors Theses. 2377.
https://scholarworks.wmich.edu/honors_theses/2377
Access Setting
Honors Thesis-Open Access
Powerpoint Presentation